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recombinant soluble fractalkine  (R&D Systems)


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    R&D Systems recombinant soluble fractalkine
    ABR threshold shifts at 1 DPNE and 15 DPNE. (A) Study design created with BioRender.com . ROA, Route of Administration. (B–F) ABR threshold shifts at 1-day post-noise exposure (DPNE) and 15 DPNE after 2 h at 93 dB SPL at 8–16 kHz octave band noise in (B) FKN WT mice treated with vehicle ( N = 8), and in FKN KO mice treated with (C) vehicle ( N = 6) (D) control peptide ( N = 7) (E) membrane-bound FKN peptide (mFKN) ( N = 9) and (F) soluble FKN peptide <t>(sFKN)</t> ( N = 8). Dashed line represents threshold shifts prior to noise exposure (baseline). Values are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant at respective stimulus frequency. *Represents comparison between 1 DPNE and 15 DPNE, two-way ANOVA, Sidak’s multiple comparisons. (G) Mean ABR threshold shift recovery at 15 DPNE of all the experimental groups. Values are means ± SD. ** p < 0.01 and ns, non-significant at respective stimulus frequency. *Represents comparison between FKN WT; vehicle (black circle) versus all other treatment groups, two-way ANOVA, Dunnett’s multiple comparisons.
    Recombinant Soluble Fractalkine, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+soluble+fractalkine/pmc11557324-52-0-3?v=R%26D+Systems
    Average 92 stars, based on 5 article reviews
    recombinant soluble fractalkine - by Bioz Stars, 2026-08
    92/100 stars

    Images

    1) Product Images from "Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy"

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2024.1486740

    ABR threshold shifts at 1 DPNE and 15 DPNE. (A) Study design created with BioRender.com . ROA, Route of Administration. (B–F) ABR threshold shifts at 1-day post-noise exposure (DPNE) and 15 DPNE after 2 h at 93 dB SPL at 8–16 kHz octave band noise in (B) FKN WT mice treated with vehicle ( N = 8), and in FKN KO mice treated with (C) vehicle ( N = 6) (D) control peptide ( N = 7) (E) membrane-bound FKN peptide (mFKN) ( N = 9) and (F) soluble FKN peptide (sFKN) ( N = 8). Dashed line represents threshold shifts prior to noise exposure (baseline). Values are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant at respective stimulus frequency. *Represents comparison between 1 DPNE and 15 DPNE, two-way ANOVA, Sidak’s multiple comparisons. (G) Mean ABR threshold shift recovery at 15 DPNE of all the experimental groups. Values are means ± SD. ** p < 0.01 and ns, non-significant at respective stimulus frequency. *Represents comparison between FKN WT; vehicle (black circle) versus all other treatment groups, two-way ANOVA, Dunnett’s multiple comparisons.
    Figure Legend Snippet: ABR threshold shifts at 1 DPNE and 15 DPNE. (A) Study design created with BioRender.com . ROA, Route of Administration. (B–F) ABR threshold shifts at 1-day post-noise exposure (DPNE) and 15 DPNE after 2 h at 93 dB SPL at 8–16 kHz octave band noise in (B) FKN WT mice treated with vehicle ( N = 8), and in FKN KO mice treated with (C) vehicle ( N = 6) (D) control peptide ( N = 7) (E) membrane-bound FKN peptide (mFKN) ( N = 9) and (F) soluble FKN peptide (sFKN) ( N = 8). Dashed line represents threshold shifts prior to noise exposure (baseline). Values are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant at respective stimulus frequency. *Represents comparison between 1 DPNE and 15 DPNE, two-way ANOVA, Sidak’s multiple comparisons. (G) Mean ABR threshold shift recovery at 15 DPNE of all the experimental groups. Values are means ± SD. ** p < 0.01 and ns, non-significant at respective stimulus frequency. *Represents comparison between FKN WT; vehicle (black circle) versus all other treatment groups, two-way ANOVA, Dunnett’s multiple comparisons.

    Techniques Used: Control, Membrane, Comparison

    ABR peak I amplitude in FKN KO mice. ABR peak I amplitudes at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN KO mice treated with (A) vehicle ( N = 6) (B) control peptide (N = 7) (C) membrane-bound FKN peptide (mFKN) ( N = 10) and (D) soluble FKN peptide (sFKN) ( N = 8). Values are means ± SD. *** p < 0.001, **** p < 0.0001, and ns, non-significant. The symbol * represents the comparison between the experimental time points as indicated with parenthesis. One-way ANOVA, Tukey’s multiple comparison test.
    Figure Legend Snippet: ABR peak I amplitude in FKN KO mice. ABR peak I amplitudes at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN KO mice treated with (A) vehicle ( N = 6) (B) control peptide (N = 7) (C) membrane-bound FKN peptide (mFKN) ( N = 10) and (D) soluble FKN peptide (sFKN) ( N = 8). Values are means ± SD. *** p < 0.001, **** p < 0.0001, and ns, non-significant. The symbol * represents the comparison between the experimental time points as indicated with parenthesis. One-way ANOVA, Tukey’s multiple comparison test.

    Techniques Used: Control, Membrane, Comparison

    Inner hair cell ribbon synapses in basal cochlear region of FKN KO mice. (A) Representative micrographs showing IHC-paired ribbon synapses in the basal cochlear region after 15 days of synaptopathic noise exposure. (B) CtBP2 puncta per IHC. (C) GluA2 puncta per IHC. (D) Paired ribbon synapses per IHC. Values are mean ± SD. Each dot in the graphs represents one mouse. Three confocal images were captured from the basal cochlear region per mouse. CtBP2 puncta, GluA2 puncta, and paired synapses per IHC were averaged across the three images per mouse and plotted. ** p < 0.01 between no noise-exposed (NNE) vs. noise-exposed vehicle-treated FKN WT and FKN KO mice; * p < 0.05 between noise-exposed FKN KO mice treated with vehicle or sFKN peptide; ns: non-significant between NNE and NE sFKN-treated FKN KO mice. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–9 mice per experimental group.
    Figure Legend Snippet: Inner hair cell ribbon synapses in basal cochlear region of FKN KO mice. (A) Representative micrographs showing IHC-paired ribbon synapses in the basal cochlear region after 15 days of synaptopathic noise exposure. (B) CtBP2 puncta per IHC. (C) GluA2 puncta per IHC. (D) Paired ribbon synapses per IHC. Values are mean ± SD. Each dot in the graphs represents one mouse. Three confocal images were captured from the basal cochlear region per mouse. CtBP2 puncta, GluA2 puncta, and paired synapses per IHC were averaged across the three images per mouse and plotted. ** p < 0.01 between no noise-exposed (NNE) vs. noise-exposed vehicle-treated FKN WT and FKN KO mice; * p < 0.05 between noise-exposed FKN KO mice treated with vehicle or sFKN peptide; ns: non-significant between NNE and NE sFKN-treated FKN KO mice. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–9 mice per experimental group.

    Techniques Used: Comparison

    ABR peak I amplitude and IHC ribbon synapse density in FKN WT mice. (A) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with vehicle. (B) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with a single dose of sFKN peptide. N = 15 mice (PNE and 1 DPNE), N = 8 mice (15 DPNE) in A and B. (C) Representative micrographs showing IHC ribbon synapses from basal cochlear region at 15 DPNE. (D) Paired ribbon synapses per IHC. (E) CtBP2 puncta per IHC. (F) GluA2 puncta per IHC. Values are means ± SD. N = 5–8 mice per experimental group. Each dot in graphs (D–F) represents one mouse. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant. One-way ANOVA, Tukey’s multiple comparison test.
    Figure Legend Snippet: ABR peak I amplitude and IHC ribbon synapse density in FKN WT mice. (A) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with vehicle. (B) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with a single dose of sFKN peptide. N = 15 mice (PNE and 1 DPNE), N = 8 mice (15 DPNE) in A and B. (C) Representative micrographs showing IHC ribbon synapses from basal cochlear region at 15 DPNE. (D) Paired ribbon synapses per IHC. (E) CtBP2 puncta per IHC. (F) GluA2 puncta per IHC. Values are means ± SD. N = 5–8 mice per experimental group. Each dot in graphs (D–F) represents one mouse. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant. One-way ANOVA, Tukey’s multiple comparison test.

    Techniques Used: Comparison

    sFKN fails to restore noise-damaged IHC ribbon synapses and ABR Peak I amplitudes in FKN WT mice lacking cochlear resident macrophages. (A) Macrophage density in the sensory epithelium of apex, middle, and basal cochlear regions of unexposed and noise-exposed FKN WT and FKN KO mice. Two-way ANOVA, Tukey’s comparison test. N = 3 mice per genotype. (B) Representative micrographs showing CD45-immunolabeled macrophages in the sensory epithelium of the middle cochlear region of unexposed and noise-exposed FKN WT and FKN KO mice. (C) Representative micrographs showing IHC-paired ribbon synapses from the basal cochlear region of vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. (D) Quantification of paired ribbon synapses per IHC in vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. Gray bar represents unexposed (NNE) FKN WT mice data re-represented from for comparison purposes and to reduce the use of mice as per IACUC policies. Two-way ANOVA, Tukey’s comparison test. (E,F) ABR Peak I amplitudes at 32 kHz in vehicle- or sFKN peptide-treated FKN WT mice in the absence [PLX5622 chow (E)] or presence [control chow (F)] of macrophages at 15 DPNE. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–7 mice per experimental group (D,E). Values are means ± SD in D or means ± SEM in (E,F). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant.
    Figure Legend Snippet: sFKN fails to restore noise-damaged IHC ribbon synapses and ABR Peak I amplitudes in FKN WT mice lacking cochlear resident macrophages. (A) Macrophage density in the sensory epithelium of apex, middle, and basal cochlear regions of unexposed and noise-exposed FKN WT and FKN KO mice. Two-way ANOVA, Tukey’s comparison test. N = 3 mice per genotype. (B) Representative micrographs showing CD45-immunolabeled macrophages in the sensory epithelium of the middle cochlear region of unexposed and noise-exposed FKN WT and FKN KO mice. (C) Representative micrographs showing IHC-paired ribbon synapses from the basal cochlear region of vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. (D) Quantification of paired ribbon synapses per IHC in vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. Gray bar represents unexposed (NNE) FKN WT mice data re-represented from for comparison purposes and to reduce the use of mice as per IACUC policies. Two-way ANOVA, Tukey’s comparison test. (E,F) ABR Peak I amplitudes at 32 kHz in vehicle- or sFKN peptide-treated FKN WT mice in the absence [PLX5622 chow (E)] or presence [control chow (F)] of macrophages at 15 DPNE. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–7 mice per experimental group (D,E). Values are means ± SD in D or means ± SEM in (E,F). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant.

    Techniques Used: Comparison, Immunolabeling, Control

    sFKN peptide modulates cochlear inflammation profile after NICS. Luminex assay-based quantification of the levels of cytokines (A) IFN- β , (B) IL-2, (C) IL-6, (D) IL-23, (E) IL-22, (F) IL-10, and (G) IL-33 in cochlear lysate from FKN WT mice subjected to either no-noise (NNE) or noise-exposed, then TT injected with vehicle at 1-day post-exposure (NE; vehicle) or noise-exposed and TT injected with sFKN peptide at 1-day post-exposure (NE; sFKN). N = 3–4 biological replicates per experimental group. Each biological sample was a pool of five cochleae run in triplicate. Values are means ± SD. * p < 0.05, **** p < 0.001, NNE vs. NE; vehicle or NE; sFKN vs. NE; vehicle. There was no significant difference in the means between NNE and NE; sFKN experimental groups. One-way ANOVA, Dunnett’s multiple comparison test.
    Figure Legend Snippet: sFKN peptide modulates cochlear inflammation profile after NICS. Luminex assay-based quantification of the levels of cytokines (A) IFN- β , (B) IL-2, (C) IL-6, (D) IL-23, (E) IL-22, (F) IL-10, and (G) IL-33 in cochlear lysate from FKN WT mice subjected to either no-noise (NNE) or noise-exposed, then TT injected with vehicle at 1-day post-exposure (NE; vehicle) or noise-exposed and TT injected with sFKN peptide at 1-day post-exposure (NE; sFKN). N = 3–4 biological replicates per experimental group. Each biological sample was a pool of five cochleae run in triplicate. Values are means ± SD. * p < 0.05, **** p < 0.001, NNE vs. NE; vehicle or NE; sFKN vs. NE; vehicle. There was no significant difference in the means between NNE and NE; sFKN experimental groups. One-way ANOVA, Dunnett’s multiple comparison test.

    Techniques Used: Luminex, Injection, Comparison

    Temporal and spatial bioavailability of sFKN peptide after TT injection in FKN KO and FKN WT mice. Estimation of levels of sFKN peptide in (A) cochlear protein lysate by ELISA and (B) cochlear perilymph by MALDI-TOF-MS at different time points after TT injection in FKN KO mice. Values are means ± SD. N = 2 biological replicates per time point after TT injection and uninjected group. (C) Representative MALDI-TOF mass spectrometric peaks of sFKN peptide (9.3 kDa) at 3 h after injection in FKN KO mice when compared to uninjected ear (blue bar). Peaks in the bottom panel represent that of the standard sFKN peptide of 9.3 kDa as positive control. Peaks of the left represent that of insulin peptide as internal control (black bar). (D) Upper panel , representative images of cochlear mid-modiolar cross section at low magnification. Bottom panel , representative images at higher magnification of the basal cochlear turn (white rectangular box in upper panel) showing the localization of fluorescent conjugated sFKN-647 (magenta) to the basilar membrane near the sensory epithelium, spiral limbus, osseous spiral lamina, and spiral ligament of uninjected and injected FKN WT mice. CD45-immunolabeled macrophages (white arrows) are found to be adhered to the undersurface of the basilar membrane among the mesothelial cells in the injected cochlea.
    Figure Legend Snippet: Temporal and spatial bioavailability of sFKN peptide after TT injection in FKN KO and FKN WT mice. Estimation of levels of sFKN peptide in (A) cochlear protein lysate by ELISA and (B) cochlear perilymph by MALDI-TOF-MS at different time points after TT injection in FKN KO mice. Values are means ± SD. N = 2 biological replicates per time point after TT injection and uninjected group. (C) Representative MALDI-TOF mass spectrometric peaks of sFKN peptide (9.3 kDa) at 3 h after injection in FKN KO mice when compared to uninjected ear (blue bar). Peaks in the bottom panel represent that of the standard sFKN peptide of 9.3 kDa as positive control. Peaks of the left represent that of insulin peptide as internal control (black bar). (D) Upper panel , representative images of cochlear mid-modiolar cross section at low magnification. Bottom panel , representative images at higher magnification of the basal cochlear turn (white rectangular box in upper panel) showing the localization of fluorescent conjugated sFKN-647 (magenta) to the basilar membrane near the sensory epithelium, spiral limbus, osseous spiral lamina, and spiral ligament of uninjected and injected FKN WT mice. CD45-immunolabeled macrophages (white arrows) are found to be adhered to the undersurface of the basilar membrane among the mesothelial cells in the injected cochlea.

    Techniques Used: Injection, Enzyme-linked Immunosorbent Assay, Positive Control, Control, Membrane, Immunolabeling

    Working model for soluble FKN restores IHC ribbon synapses after NICS. Prolonged or loud exposure to noise results in rapid loss of IHC ribbon synapses known as cochlear synaptopathy. Locally (transtympanically) delivered immune factor, soluble FKN reaches into the cochlea near the sensory epithelium and is effective in restoring the noise-induced loss of IHC ribbon synapses and hearing via cochlear macrophages expressing CX 3 CR1 and suppresses cochlear inflammation in response to noise insult. The precise mechanisms by which sFKN–macrophage interactions contribute to synaptic and functional recovery remain to be elucidated. The figure was created with BioRender.com .
    Figure Legend Snippet: Working model for soluble FKN restores IHC ribbon synapses after NICS. Prolonged or loud exposure to noise results in rapid loss of IHC ribbon synapses known as cochlear synaptopathy. Locally (transtympanically) delivered immune factor, soluble FKN reaches into the cochlea near the sensory epithelium and is effective in restoring the noise-induced loss of IHC ribbon synapses and hearing via cochlear macrophages expressing CX 3 CR1 and suppresses cochlear inflammation in response to noise insult. The precise mechanisms by which sFKN–macrophage interactions contribute to synaptic and functional recovery remain to be elucidated. The figure was created with BioRender.com .

    Techniques Used: Expressing, Functional Assay



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    Image Search Results


    ABR threshold shifts at 1 DPNE and 15 DPNE. (A) Study design created with BioRender.com . ROA, Route of Administration. (B–F) ABR threshold shifts at 1-day post-noise exposure (DPNE) and 15 DPNE after 2 h at 93 dB SPL at 8–16 kHz octave band noise in (B) FKN WT mice treated with vehicle ( N = 8), and in FKN KO mice treated with (C) vehicle ( N = 6) (D) control peptide ( N = 7) (E) membrane-bound FKN peptide (mFKN) ( N = 9) and (F) soluble FKN peptide (sFKN) ( N = 8). Dashed line represents threshold shifts prior to noise exposure (baseline). Values are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant at respective stimulus frequency. *Represents comparison between 1 DPNE and 15 DPNE, two-way ANOVA, Sidak’s multiple comparisons. (G) Mean ABR threshold shift recovery at 15 DPNE of all the experimental groups. Values are means ± SD. ** p < 0.01 and ns, non-significant at respective stimulus frequency. *Represents comparison between FKN WT; vehicle (black circle) versus all other treatment groups, two-way ANOVA, Dunnett’s multiple comparisons.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: ABR threshold shifts at 1 DPNE and 15 DPNE. (A) Study design created with BioRender.com . ROA, Route of Administration. (B–F) ABR threshold shifts at 1-day post-noise exposure (DPNE) and 15 DPNE after 2 h at 93 dB SPL at 8–16 kHz octave band noise in (B) FKN WT mice treated with vehicle ( N = 8), and in FKN KO mice treated with (C) vehicle ( N = 6) (D) control peptide ( N = 7) (E) membrane-bound FKN peptide (mFKN) ( N = 9) and (F) soluble FKN peptide (sFKN) ( N = 8). Dashed line represents threshold shifts prior to noise exposure (baseline). Values are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant at respective stimulus frequency. *Represents comparison between 1 DPNE and 15 DPNE, two-way ANOVA, Sidak’s multiple comparisons. (G) Mean ABR threshold shift recovery at 15 DPNE of all the experimental groups. Values are means ± SD. ** p < 0.01 and ns, non-significant at respective stimulus frequency. *Represents comparison between FKN WT; vehicle (black circle) versus all other treatment groups, two-way ANOVA, Dunnett’s multiple comparisons.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Control, Membrane, Comparison

    ABR peak I amplitude in FKN KO mice. ABR peak I amplitudes at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN KO mice treated with (A) vehicle ( N = 6) (B) control peptide (N = 7) (C) membrane-bound FKN peptide (mFKN) ( N = 10) and (D) soluble FKN peptide (sFKN) ( N = 8). Values are means ± SD. *** p < 0.001, **** p < 0.0001, and ns, non-significant. The symbol * represents the comparison between the experimental time points as indicated with parenthesis. One-way ANOVA, Tukey’s multiple comparison test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: ABR peak I amplitude in FKN KO mice. ABR peak I amplitudes at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN KO mice treated with (A) vehicle ( N = 6) (B) control peptide (N = 7) (C) membrane-bound FKN peptide (mFKN) ( N = 10) and (D) soluble FKN peptide (sFKN) ( N = 8). Values are means ± SD. *** p < 0.001, **** p < 0.0001, and ns, non-significant. The symbol * represents the comparison between the experimental time points as indicated with parenthesis. One-way ANOVA, Tukey’s multiple comparison test.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Control, Membrane, Comparison

    Inner hair cell ribbon synapses in basal cochlear region of FKN KO mice. (A) Representative micrographs showing IHC-paired ribbon synapses in the basal cochlear region after 15 days of synaptopathic noise exposure. (B) CtBP2 puncta per IHC. (C) GluA2 puncta per IHC. (D) Paired ribbon synapses per IHC. Values are mean ± SD. Each dot in the graphs represents one mouse. Three confocal images were captured from the basal cochlear region per mouse. CtBP2 puncta, GluA2 puncta, and paired synapses per IHC were averaged across the three images per mouse and plotted. ** p < 0.01 between no noise-exposed (NNE) vs. noise-exposed vehicle-treated FKN WT and FKN KO mice; * p < 0.05 between noise-exposed FKN KO mice treated with vehicle or sFKN peptide; ns: non-significant between NNE and NE sFKN-treated FKN KO mice. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–9 mice per experimental group.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: Inner hair cell ribbon synapses in basal cochlear region of FKN KO mice. (A) Representative micrographs showing IHC-paired ribbon synapses in the basal cochlear region after 15 days of synaptopathic noise exposure. (B) CtBP2 puncta per IHC. (C) GluA2 puncta per IHC. (D) Paired ribbon synapses per IHC. Values are mean ± SD. Each dot in the graphs represents one mouse. Three confocal images were captured from the basal cochlear region per mouse. CtBP2 puncta, GluA2 puncta, and paired synapses per IHC were averaged across the three images per mouse and plotted. ** p < 0.01 between no noise-exposed (NNE) vs. noise-exposed vehicle-treated FKN WT and FKN KO mice; * p < 0.05 between noise-exposed FKN KO mice treated with vehicle or sFKN peptide; ns: non-significant between NNE and NE sFKN-treated FKN KO mice. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–9 mice per experimental group.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Comparison

    ABR peak I amplitude and IHC ribbon synapse density in FKN WT mice. (A) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with vehicle. (B) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with a single dose of sFKN peptide. N = 15 mice (PNE and 1 DPNE), N = 8 mice (15 DPNE) in A and B. (C) Representative micrographs showing IHC ribbon synapses from basal cochlear region at 15 DPNE. (D) Paired ribbon synapses per IHC. (E) CtBP2 puncta per IHC. (F) GluA2 puncta per IHC. Values are means ± SD. N = 5–8 mice per experimental group. Each dot in graphs (D–F) represents one mouse. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant. One-way ANOVA, Tukey’s multiple comparison test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: ABR peak I amplitude and IHC ribbon synapse density in FKN WT mice. (A) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with vehicle. (B) ABR peak I amplitude at 32 kHz at pre-noise exposure (PNE), 1 DPNE, and 15 DPNE in FKN WT mice treated with a single dose of sFKN peptide. N = 15 mice (PNE and 1 DPNE), N = 8 mice (15 DPNE) in A and B. (C) Representative micrographs showing IHC ribbon synapses from basal cochlear region at 15 DPNE. (D) Paired ribbon synapses per IHC. (E) CtBP2 puncta per IHC. (F) GluA2 puncta per IHC. Values are means ± SD. N = 5–8 mice per experimental group. Each dot in graphs (D–F) represents one mouse. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant. One-way ANOVA, Tukey’s multiple comparison test.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Comparison

    sFKN fails to restore noise-damaged IHC ribbon synapses and ABR Peak I amplitudes in FKN WT mice lacking cochlear resident macrophages. (A) Macrophage density in the sensory epithelium of apex, middle, and basal cochlear regions of unexposed and noise-exposed FKN WT and FKN KO mice. Two-way ANOVA, Tukey’s comparison test. N = 3 mice per genotype. (B) Representative micrographs showing CD45-immunolabeled macrophages in the sensory epithelium of the middle cochlear region of unexposed and noise-exposed FKN WT and FKN KO mice. (C) Representative micrographs showing IHC-paired ribbon synapses from the basal cochlear region of vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. (D) Quantification of paired ribbon synapses per IHC in vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. Gray bar represents unexposed (NNE) FKN WT mice data re-represented from for comparison purposes and to reduce the use of mice as per IACUC policies. Two-way ANOVA, Tukey’s comparison test. (E,F) ABR Peak I amplitudes at 32 kHz in vehicle- or sFKN peptide-treated FKN WT mice in the absence [PLX5622 chow (E)] or presence [control chow (F)] of macrophages at 15 DPNE. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–7 mice per experimental group (D,E). Values are means ± SD in D or means ± SEM in (E,F). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: sFKN fails to restore noise-damaged IHC ribbon synapses and ABR Peak I amplitudes in FKN WT mice lacking cochlear resident macrophages. (A) Macrophage density in the sensory epithelium of apex, middle, and basal cochlear regions of unexposed and noise-exposed FKN WT and FKN KO mice. Two-way ANOVA, Tukey’s comparison test. N = 3 mice per genotype. (B) Representative micrographs showing CD45-immunolabeled macrophages in the sensory epithelium of the middle cochlear region of unexposed and noise-exposed FKN WT and FKN KO mice. (C) Representative micrographs showing IHC-paired ribbon synapses from the basal cochlear region of vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. (D) Quantification of paired ribbon synapses per IHC in vehicle- or sFKN peptide-treated FKN WT mice in the presence (control chow) or absence (PLX5622 chow) of macrophages at 15 DPNE. Gray bar represents unexposed (NNE) FKN WT mice data re-represented from for comparison purposes and to reduce the use of mice as per IACUC policies. Two-way ANOVA, Tukey’s comparison test. (E,F) ABR Peak I amplitudes at 32 kHz in vehicle- or sFKN peptide-treated FKN WT mice in the absence [PLX5622 chow (E)] or presence [control chow (F)] of macrophages at 15 DPNE. One-way ANOVA, Dunnett’s multiple comparison test. N = 5–7 mice per experimental group (D,E). Values are means ± SD in D or means ± SEM in (E,F). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns, non-significant.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Comparison, Immunolabeling, Control

    sFKN peptide modulates cochlear inflammation profile after NICS. Luminex assay-based quantification of the levels of cytokines (A) IFN- β , (B) IL-2, (C) IL-6, (D) IL-23, (E) IL-22, (F) IL-10, and (G) IL-33 in cochlear lysate from FKN WT mice subjected to either no-noise (NNE) or noise-exposed, then TT injected with vehicle at 1-day post-exposure (NE; vehicle) or noise-exposed and TT injected with sFKN peptide at 1-day post-exposure (NE; sFKN). N = 3–4 biological replicates per experimental group. Each biological sample was a pool of five cochleae run in triplicate. Values are means ± SD. * p < 0.05, **** p < 0.001, NNE vs. NE; vehicle or NE; sFKN vs. NE; vehicle. There was no significant difference in the means between NNE and NE; sFKN experimental groups. One-way ANOVA, Dunnett’s multiple comparison test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: sFKN peptide modulates cochlear inflammation profile after NICS. Luminex assay-based quantification of the levels of cytokines (A) IFN- β , (B) IL-2, (C) IL-6, (D) IL-23, (E) IL-22, (F) IL-10, and (G) IL-33 in cochlear lysate from FKN WT mice subjected to either no-noise (NNE) or noise-exposed, then TT injected with vehicle at 1-day post-exposure (NE; vehicle) or noise-exposed and TT injected with sFKN peptide at 1-day post-exposure (NE; sFKN). N = 3–4 biological replicates per experimental group. Each biological sample was a pool of five cochleae run in triplicate. Values are means ± SD. * p < 0.05, **** p < 0.001, NNE vs. NE; vehicle or NE; sFKN vs. NE; vehicle. There was no significant difference in the means between NNE and NE; sFKN experimental groups. One-way ANOVA, Dunnett’s multiple comparison test.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Luminex, Injection, Comparison

    Temporal and spatial bioavailability of sFKN peptide after TT injection in FKN KO and FKN WT mice. Estimation of levels of sFKN peptide in (A) cochlear protein lysate by ELISA and (B) cochlear perilymph by MALDI-TOF-MS at different time points after TT injection in FKN KO mice. Values are means ± SD. N = 2 biological replicates per time point after TT injection and uninjected group. (C) Representative MALDI-TOF mass spectrometric peaks of sFKN peptide (9.3 kDa) at 3 h after injection in FKN KO mice when compared to uninjected ear (blue bar). Peaks in the bottom panel represent that of the standard sFKN peptide of 9.3 kDa as positive control. Peaks of the left represent that of insulin peptide as internal control (black bar). (D) Upper panel , representative images of cochlear mid-modiolar cross section at low magnification. Bottom panel , representative images at higher magnification of the basal cochlear turn (white rectangular box in upper panel) showing the localization of fluorescent conjugated sFKN-647 (magenta) to the basilar membrane near the sensory epithelium, spiral limbus, osseous spiral lamina, and spiral ligament of uninjected and injected FKN WT mice. CD45-immunolabeled macrophages (white arrows) are found to be adhered to the undersurface of the basilar membrane among the mesothelial cells in the injected cochlea.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: Temporal and spatial bioavailability of sFKN peptide after TT injection in FKN KO and FKN WT mice. Estimation of levels of sFKN peptide in (A) cochlear protein lysate by ELISA and (B) cochlear perilymph by MALDI-TOF-MS at different time points after TT injection in FKN KO mice. Values are means ± SD. N = 2 biological replicates per time point after TT injection and uninjected group. (C) Representative MALDI-TOF mass spectrometric peaks of sFKN peptide (9.3 kDa) at 3 h after injection in FKN KO mice when compared to uninjected ear (blue bar). Peaks in the bottom panel represent that of the standard sFKN peptide of 9.3 kDa as positive control. Peaks of the left represent that of insulin peptide as internal control (black bar). (D) Upper panel , representative images of cochlear mid-modiolar cross section at low magnification. Bottom panel , representative images at higher magnification of the basal cochlear turn (white rectangular box in upper panel) showing the localization of fluorescent conjugated sFKN-647 (magenta) to the basilar membrane near the sensory epithelium, spiral limbus, osseous spiral lamina, and spiral ligament of uninjected and injected FKN WT mice. CD45-immunolabeled macrophages (white arrows) are found to be adhered to the undersurface of the basilar membrane among the mesothelial cells in the injected cochlea.

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Injection, Enzyme-linked Immunosorbent Assay, Positive Control, Control, Membrane, Immunolabeling

    Working model for soluble FKN restores IHC ribbon synapses after NICS. Prolonged or loud exposure to noise results in rapid loss of IHC ribbon synapses known as cochlear synaptopathy. Locally (transtympanically) delivered immune factor, soluble FKN reaches into the cochlea near the sensory epithelium and is effective in restoring the noise-induced loss of IHC ribbon synapses and hearing via cochlear macrophages expressing CX 3 CR1 and suppresses cochlear inflammation in response to noise insult. The precise mechanisms by which sFKN–macrophage interactions contribute to synaptic and functional recovery remain to be elucidated. The figure was created with BioRender.com .

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Local delivery of soluble fractalkine (CX3CL1) peptide restores ribbon synapses after noise-induced cochlear synaptopathy

    doi: 10.3389/fncel.2024.1486740

    Figure Lengend Snippet: Working model for soluble FKN restores IHC ribbon synapses after NICS. Prolonged or loud exposure to noise results in rapid loss of IHC ribbon synapses known as cochlear synaptopathy. Locally (transtympanically) delivered immune factor, soluble FKN reaches into the cochlea near the sensory epithelium and is effective in restoring the noise-induced loss of IHC ribbon synapses and hearing via cochlear macrophages expressing CX 3 CR1 and suppresses cochlear inflammation in response to noise insult. The precise mechanisms by which sFKN–macrophage interactions contribute to synaptic and functional recovery remain to be elucidated. The figure was created with BioRender.com .

    Article Snippet: Recombinant soluble Fractalkine (R&D systems, cat. # 571-MF, Accession # AAB71763) is sourced from E. coli -derived mouse CX3CL1/Fractalkine peptide of 80 amino acids (aa 25–105) of 9.3 kDa.

    Techniques: Expressing, Functional Assay

    CX3CL1 expression in response to glucose stimulation. (A) Blood glucose levels at 3 and 42 days in streptozotocin (STZ)-induced DM mice. Insulin treatment was initiated at 28 days after STZ injection and persisted for 14 days. * p < 0.05, n = 8 in each group. (B) Blood glucose levels at 3 and 42 days in NOD mice. The NOD mice were assigned to three groups: normal glucose (NG) group (some mice didn’t develop into hyperglycemia), NOD group (with twice random blood glucose level>20 mM) and NOD&insulin group. Insulin treatment protocol was the same as panel (A) . * p < 0.05, n = 8 in each group. (C) Representative western blotting of CX3CL1 in the heart and kidney tissue of mice at various time points after STZ-injection. (D) Semi-quantitation of CX3CL1 expression in panel (C) . * p < 0.05, vs . the corresponding 0 day, n = 5 per group. (E) Immunohistochemical detection of CX3CL1 expression in heart and kidney tissues of normal or diabetic mice. Scale bar = 100 μm. (F) Cardiac CX3CL1 and CX3CR1 mRNA expression in NOD mice. (G) Renal gene expression of CX3CL1 and CX3CR1 in NOD mice. * p < 0.05, vs . NG, n = 6 per group. (H) CX3CL1 expression detected by western blotting in heart and kidney tissues from DM mice with or without insulin treatment for 14 days. (I) Semi-quantitation of CX3CL1 in panel (H) . * p < 0.05 vs . WT&Vehicle, n = 5 in each group. (J) mRNA expression of CX3CL1 in neonatal rat cardiomyocytes (NRCM) and fibroblasts (NRCF), two types of renal cell lines HBZY-1 and NRK-52E exposed to different concentrations of glucose medium for 3 days. * p < 0.05 vs . 5.5 mM group, n = 5 in each group. Experiments presented in panels (A) , (B) , (D) , (I) , and (J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test. Experiments presented in panels (F) and (G) were analyzed using two-tailed unpaired t -test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: CX3CL1 expression in response to glucose stimulation. (A) Blood glucose levels at 3 and 42 days in streptozotocin (STZ)-induced DM mice. Insulin treatment was initiated at 28 days after STZ injection and persisted for 14 days. * p < 0.05, n = 8 in each group. (B) Blood glucose levels at 3 and 42 days in NOD mice. The NOD mice were assigned to three groups: normal glucose (NG) group (some mice didn’t develop into hyperglycemia), NOD group (with twice random blood glucose level>20 mM) and NOD&insulin group. Insulin treatment protocol was the same as panel (A) . * p < 0.05, n = 8 in each group. (C) Representative western blotting of CX3CL1 in the heart and kidney tissue of mice at various time points after STZ-injection. (D) Semi-quantitation of CX3CL1 expression in panel (C) . * p < 0.05, vs . the corresponding 0 day, n = 5 per group. (E) Immunohistochemical detection of CX3CL1 expression in heart and kidney tissues of normal or diabetic mice. Scale bar = 100 μm. (F) Cardiac CX3CL1 and CX3CR1 mRNA expression in NOD mice. (G) Renal gene expression of CX3CL1 and CX3CR1 in NOD mice. * p < 0.05, vs . NG, n = 6 per group. (H) CX3CL1 expression detected by western blotting in heart and kidney tissues from DM mice with or without insulin treatment for 14 days. (I) Semi-quantitation of CX3CL1 in panel (H) . * p < 0.05 vs . WT&Vehicle, n = 5 in each group. (J) mRNA expression of CX3CL1 in neonatal rat cardiomyocytes (NRCM) and fibroblasts (NRCF), two types of renal cell lines HBZY-1 and NRK-52E exposed to different concentrations of glucose medium for 3 days. * p < 0.05 vs . 5.5 mM group, n = 5 in each group. Experiments presented in panels (A) , (B) , (D) , (I) , and (J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test. Experiments presented in panels (F) and (G) were analyzed using two-tailed unpaired t -test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Expressing, Injection, Western Blot, Quantitation Assay, Immunohistochemical staining, Gene Expression, Two Tailed Test

    sCX3CL1 promotes mitochondrial-dependent apoptosis in cardiomyocytes and renal cells. (A) Western blotting to detect RhoA and GTP-bound RhoA protein in neonatal rat cardiomyocytes (NRCM) and HBZY-1 cells after 60 min of stimulation with 200 ng/ml of sCX3CL1 (soluble CX3CL1). (B) Western blotting to detect upregulation of ROCK1 and cleaved ROCK1 (c-ROCK) expression in response to stimulation of NRCM and HBZY-1 cells with sCX3CL1 (200 ng/ml) for 24 h. (C) Semi-quantitation of RhoA-GTP, ROCK and cleaved-ROCK expression. * p < 0.05 vs . control, n = 5 in each group. Representative images of (D) calcein fluorescence or (E) TMRE fluorescence (Mitochondrial membrane potential) in cells cultured with sCX3CL1 alone or co-treated with either a CX3CR1 neutralizing antibody or a Rho kinase inhibitor (Y-27632). Scale bar = 100 μm. Semi-quantitative analysis of calcein (F) or TMRE (G) fluorescence intensity ( * p < 0.05 vs . sCX3CL1), n = 5 in each group. (H) Western blots analysis of Bax, cytochrome C (Cyto C) in NRCM and HBZY-1. Semi-quantitation analysis of Bax and Cyto C in NRCM (I) and HBZY-1 cells (J) . * p < 0.05 vs . sCX3CL1, n = 5 in each group. (K) Subcellular localization of AIF (apoptosis inducing factor) was detected in NRCM and HBZY-1 cells after sCX3CL1 stimulation or co-treatment with either a CX3CR1 neutralizing antibody or Y-27632. Scale bar = 30 μm. Experiments presented in panel (C) was analyzed using two-tailed unpaired t -test and in panels (F) , (G) , (I) , and (J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: sCX3CL1 promotes mitochondrial-dependent apoptosis in cardiomyocytes and renal cells. (A) Western blotting to detect RhoA and GTP-bound RhoA protein in neonatal rat cardiomyocytes (NRCM) and HBZY-1 cells after 60 min of stimulation with 200 ng/ml of sCX3CL1 (soluble CX3CL1). (B) Western blotting to detect upregulation of ROCK1 and cleaved ROCK1 (c-ROCK) expression in response to stimulation of NRCM and HBZY-1 cells with sCX3CL1 (200 ng/ml) for 24 h. (C) Semi-quantitation of RhoA-GTP, ROCK and cleaved-ROCK expression. * p < 0.05 vs . control, n = 5 in each group. Representative images of (D) calcein fluorescence or (E) TMRE fluorescence (Mitochondrial membrane potential) in cells cultured with sCX3CL1 alone or co-treated with either a CX3CR1 neutralizing antibody or a Rho kinase inhibitor (Y-27632). Scale bar = 100 μm. Semi-quantitative analysis of calcein (F) or TMRE (G) fluorescence intensity ( * p < 0.05 vs . sCX3CL1), n = 5 in each group. (H) Western blots analysis of Bax, cytochrome C (Cyto C) in NRCM and HBZY-1. Semi-quantitation analysis of Bax and Cyto C in NRCM (I) and HBZY-1 cells (J) . * p < 0.05 vs . sCX3CL1, n = 5 in each group. (K) Subcellular localization of AIF (apoptosis inducing factor) was detected in NRCM and HBZY-1 cells after sCX3CL1 stimulation or co-treatment with either a CX3CR1 neutralizing antibody or Y-27632. Scale bar = 30 μm. Experiments presented in panel (C) was analyzed using two-tailed unpaired t -test and in panels (F) , (G) , (I) , and (J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Western Blot, Expressing, Quantitation Assay, Control, Fluorescence, Membrane, Cell Culture, Two Tailed Test

    Effect of CX3CL1/CX3CR1 inhibition on cardiorenal dysfunction in mice with diabetes-induced CRS. (A) Representative M-mode echocardiographic images of mice at 6 weeks after STZ injection. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (B) Left ventricular fractional shortening (LVFS). (C) Microalbuminuria amount for 24 h. (D) Serum creatinine levels. (E) Serum NGAL levels. For panels (B–E) , * p < 0.05 vs . WT&STZ group; † p < 0.05 vs . WT&STZ&Insulin group. For panel (B) , n = 6 in WT&Vehicle, WT&STZ&Inuslin, and CX3CR1 −/− &Vehicle group; n = 7 in WT&STZ and CX3CR1 −/− &STZ group; n = 5 in WT&STZ&anti-CX3CL1 group. n = 5 per group in panels (C–E) . (F) Representative M-mode echocardiographic images. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (G) LVFS. (H) Concentrations of serum BUN (urea nitrogen). (I) Serum creatinine levels. (J) Urine creatinine levels. For panel (G–J) , * p < 0.05 vs . NOD&Vehicle group. In panel (G) , n = 8 in NG&Vehicle; n = 6 in NOD&Vehicle, NOD&sh-scr, and NOD&sh-CX3CR1 group; n = 7 in NOD&Inuslin; n = 5 in NOD&Anti-CX3CL1. n = 6 per group in panel (H) ; n = 5 per group in panels (I–J) . Experiments presented in panels (B–E) and (G–J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: Effect of CX3CL1/CX3CR1 inhibition on cardiorenal dysfunction in mice with diabetes-induced CRS. (A) Representative M-mode echocardiographic images of mice at 6 weeks after STZ injection. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (B) Left ventricular fractional shortening (LVFS). (C) Microalbuminuria amount for 24 h. (D) Serum creatinine levels. (E) Serum NGAL levels. For panels (B–E) , * p < 0.05 vs . WT&STZ group; † p < 0.05 vs . WT&STZ&Insulin group. For panel (B) , n = 6 in WT&Vehicle, WT&STZ&Inuslin, and CX3CR1 −/− &Vehicle group; n = 7 in WT&STZ and CX3CR1 −/− &STZ group; n = 5 in WT&STZ&anti-CX3CL1 group. n = 5 per group in panels (C–E) . (F) Representative M-mode echocardiographic images. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (G) LVFS. (H) Concentrations of serum BUN (urea nitrogen). (I) Serum creatinine levels. (J) Urine creatinine levels. For panel (G–J) , * p < 0.05 vs . NOD&Vehicle group. In panel (G) , n = 8 in NG&Vehicle; n = 6 in NOD&Vehicle, NOD&sh-scr, and NOD&sh-CX3CR1 group; n = 7 in NOD&Inuslin; n = 5 in NOD&Anti-CX3CL1. n = 6 per group in panel (H) ; n = 5 per group in panels (I–J) . Experiments presented in panels (B–E) and (G–J) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Inhibition, Injection

    Inhibition of CX3CL1/CX3CR1 attenuated apoptosis in mice with STZ-induced diabetes. (A) Representative images of TUNEL staining in heart sections at 6 weeks after STZ-injection. (B) Percentage of TUNEL-positive nuclei in heart tissue. (C) Representative images of TUNEL staining in kidney sections at 6 weeks after STZ-injection. (D) Percentage of TUNEL-positive nuclei in kidney tissue. (E) Bax immunostaining (brown staining) in heart tissue. (F) Bax immunostaining in kidney tissue. (G) Representative electronic micrographs of the heart featuring sarcomeres and mitochondria. (H) Representative electronic micrographs of the kidney featuring tubular mitochondria. For panel (B) and (D) , * p < 0.05 vs . WT&STZ mice; † p < 0.05 vs . WT&STZ&Insulin mice, n = 5 in each group. Scale bar = 100 μm in panel (A) and (C) , Scale bar = 1 μm in panel (G) and (H) . Experiments presented in panels (B) and (D) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: Inhibition of CX3CL1/CX3CR1 attenuated apoptosis in mice with STZ-induced diabetes. (A) Representative images of TUNEL staining in heart sections at 6 weeks after STZ-injection. (B) Percentage of TUNEL-positive nuclei in heart tissue. (C) Representative images of TUNEL staining in kidney sections at 6 weeks after STZ-injection. (D) Percentage of TUNEL-positive nuclei in kidney tissue. (E) Bax immunostaining (brown staining) in heart tissue. (F) Bax immunostaining in kidney tissue. (G) Representative electronic micrographs of the heart featuring sarcomeres and mitochondria. (H) Representative electronic micrographs of the kidney featuring tubular mitochondria. For panel (B) and (D) , * p < 0.05 vs . WT&STZ mice; † p < 0.05 vs . WT&STZ&Insulin mice, n = 5 in each group. Scale bar = 100 μm in panel (A) and (C) , Scale bar = 1 μm in panel (G) and (H) . Experiments presented in panels (B) and (D) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Inhibition, TUNEL Assay, Staining, Injection, Immunostaining, Mouse Assay

    Inhibition of CX3CL1/CX3CR1 attenuated fibrosis in diabetes mice. (A) Myocardial interstitial fibrosis in STZ-induced DM mice. (B) Perivascular fibrosis of heart in STZ-induced DM mice. (C) Fibrotic score of the renal interstitial area in STZ-induced DM mice. (D) Fibrotic score of the glomeruli area in STZ-induced DM mice. (E) Myocardial interstitial fibrosis in NOD mice. (F) Perivascular fibrosis of heart in NOD mice. (G) Fibrotic score of the renal interstitial area in NOD mice. (H) Fibrotic score of the glomeruli area in NOD mice. (I) Representative images of immunostaining for DAPI (blue), α-SMA (green) and vimentin (red) in heart tissue. Scale bar = 100 μm. (J) Representative images of immunostaining for E-cadherin (red), fibronectin (red), vimentin (red), and α-SMA (green) in kidney tissue. Scale bar = 100 μm. For panels (A–D) , * p < 0.05 vs . WT&STZ group; † p < 0.05 vs . WT&STZ&Insulin mice; n = 5 per group. For panels (E–H) , * p < 0.05 vs . NOD&Vehicle group; n = 6 per group. Experiments presented in panels (A–H) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: Inhibition of CX3CL1/CX3CR1 attenuated fibrosis in diabetes mice. (A) Myocardial interstitial fibrosis in STZ-induced DM mice. (B) Perivascular fibrosis of heart in STZ-induced DM mice. (C) Fibrotic score of the renal interstitial area in STZ-induced DM mice. (D) Fibrotic score of the glomeruli area in STZ-induced DM mice. (E) Myocardial interstitial fibrosis in NOD mice. (F) Perivascular fibrosis of heart in NOD mice. (G) Fibrotic score of the renal interstitial area in NOD mice. (H) Fibrotic score of the glomeruli area in NOD mice. (I) Representative images of immunostaining for DAPI (blue), α-SMA (green) and vimentin (red) in heart tissue. Scale bar = 100 μm. (J) Representative images of immunostaining for E-cadherin (red), fibronectin (red), vimentin (red), and α-SMA (green) in kidney tissue. Scale bar = 100 μm. For panels (A–D) , * p < 0.05 vs . WT&STZ group; † p < 0.05 vs . WT&STZ&Insulin mice; n = 5 per group. For panels (E–H) , * p < 0.05 vs . NOD&Vehicle group; n = 6 per group. Experiments presented in panels (A–H) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Inhibition, Immunostaining

    Canagliflozin (Cana) improved cardiorenal dysfunction and repressed diabetic induced or high glucose induced CX3CL1 expression. (A) M-mode of echocardiography. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (B) Left ventricular fractional shortening (LVFS). (C) Serum creatinine concentration. (D) Renal neutrophil gelatinase-associated lipocalin (NGAL) content. (E) CX3CL1 expression detected by Western blotting in heart and kidney tissues. (F) Semi-quantitation of CX3CL1 expression in heart. (G) Semi-quantitation of CX3CL1 expression in kidney. * p < 0.05 vs . WT&STZ mice; n = 6 per group. (H–M) Western blotting of CX3CL1 levels in cultured cardiomyocytes (H9C2), glomerular mesangial cells (HBZY-1), neonatal rat cardiac fibroblasts (NRCF) and renal tubular epithelial cells (NRK-52E). The cultured cells were exposed for 5 days either to normal concentration of glucose (5 mM, NG) or high concentration of glucose (33.3 mM, HG) as well as to HG for 3 days followed by NG for 2 days (HN) with/without treatment of Cana. * p < 0.05 vs . HG; † p < 0.05 vs . HN; n = 5 per group. Experiments presented in panels (B–D) , (F–G) , (I–J) , and (L–M) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: Canagliflozin (Cana) improved cardiorenal dysfunction and repressed diabetic induced or high glucose induced CX3CL1 expression. (A) M-mode of echocardiography. Scale bars, 2 mm (upper panels), horizontal bars represent 100 ms. (B) Left ventricular fractional shortening (LVFS). (C) Serum creatinine concentration. (D) Renal neutrophil gelatinase-associated lipocalin (NGAL) content. (E) CX3CL1 expression detected by Western blotting in heart and kidney tissues. (F) Semi-quantitation of CX3CL1 expression in heart. (G) Semi-quantitation of CX3CL1 expression in kidney. * p < 0.05 vs . WT&STZ mice; n = 6 per group. (H–M) Western blotting of CX3CL1 levels in cultured cardiomyocytes (H9C2), glomerular mesangial cells (HBZY-1), neonatal rat cardiac fibroblasts (NRCF) and renal tubular epithelial cells (NRK-52E). The cultured cells were exposed for 5 days either to normal concentration of glucose (5 mM, NG) or high concentration of glucose (33.3 mM, HG) as well as to HG for 3 days followed by NG for 2 days (HN) with/without treatment of Cana. * p < 0.05 vs . HG; † p < 0.05 vs . HN; n = 5 per group. Experiments presented in panels (B–D) , (F–G) , (I–J) , and (L–M) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Expressing, Concentration Assay, Western Blot, Quantitation Assay, Cell Culture

    Illustration of the molecular mechanisms by which CX3CL1 promotes cardiorenal dysfunction induced by diabetics. CX3CL1 expression is upregulated in cardiac and renal cells by a high glucose environment. Persistent high CX3CL1 expression accelerates the mitochondrial apoptotic pathway through activation of RhoA/ROCK1-Bax signaling. In addition, CX3CL1 regulates fibroblast and epithelial cell phenotypic trans-differentiation through activation of TGF-β/Smad signaling. CX3CL1 leads to the onset of cardiorenal dysfunction in diabetes-induced cardiorenal syndrome type 5 (CRS5) due to its proapoptotic and profibrotic effects, while SGLT2 inhibitor could improve CRS5 at least partially by repressing CX3CL1 expression.

    Journal: Frontiers in Pharmacology

    Article Title: CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome

    doi: 10.3389/fphar.2022.848310

    Figure Lengend Snippet: Illustration of the molecular mechanisms by which CX3CL1 promotes cardiorenal dysfunction induced by diabetics. CX3CL1 expression is upregulated in cardiac and renal cells by a high glucose environment. Persistent high CX3CL1 expression accelerates the mitochondrial apoptotic pathway through activation of RhoA/ROCK1-Bax signaling. In addition, CX3CL1 regulates fibroblast and epithelial cell phenotypic trans-differentiation through activation of TGF-β/Smad signaling. CX3CL1 leads to the onset of cardiorenal dysfunction in diabetes-induced cardiorenal syndrome type 5 (CRS5) due to its proapoptotic and profibrotic effects, while SGLT2 inhibitor could improve CRS5 at least partially by repressing CX3CL1 expression.

    Article Snippet: Cultured NRCM and HBZY-1 were starved of serum for 12 h and then were exposed to recombinant soluble CX3CL1 (chemokine domain; 537-FT-025; R&D) at 200 ng/ml for 24 h in the presence or absence of 10 μM Y27632 (a ROCK inhibitor; Selleck) or 5 μg/ml of an anti-CX3CR1 antibody (GTX27200; Genetex).

    Techniques: Expressing, Activation Assay

    FIGURE 1. CX3CL1 secreted by MSCs. ELISA analysis indi- cated that secretion of CX3CL1 from CX3CL1-MSCs was signifi- cantly higher than that from other MSCs groups, while CX3CL1 neutralizing antibody could downregulate CX3CL1 secretion by MSCs. The concentration of CX3CL1 in culture medium was not significantly different among normal MSCs, GFP-MSCs and the control treated with isotype antibody. Values are mean ± SD. n = 6, *P < 0.05, **P < 0.01.

    Journal: Ocular immunology and inflammation

    Article Title: Mesenchymal Stem Cells Modulate Light-induced Activation of Retinal Microglia Through CX3CL1/CX3CR1 Signaling.

    doi: 10.3109/09273948.2015.1071405

    Figure Lengend Snippet: FIGURE 1. CX3CL1 secreted by MSCs. ELISA analysis indi- cated that secretion of CX3CL1 from CX3CL1-MSCs was signifi- cantly higher than that from other MSCs groups, while CX3CL1 neutralizing antibody could downregulate CX3CL1 secretion by MSCs. The concentration of CX3CL1 in culture medium was not significantly different among normal MSCs, GFP-MSCs and the control treated with isotype antibody. Values are mean ± SD. n = 6, *P < 0.05, **P < 0.01.

    Article Snippet: The rat recombinant soluble CX3CL1 protein (5 ng/mL, R&D, USA) was directly added to microglia culture upon ISHR stimulation for 24 h, and the protein expression of CNTF, BDNF, CX3CR1, IL-1β, and TNF-α was detected by Western blot.

    Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Control

    FIGURE 3. MSCs coculture affects the protein expression of cytokines by activated microglia. Western blot analyses showed that cocultured with MSCs inhibit the expression of TNF-α and IL-1β by activated microglia (A). Notably, CX3CL1-MSCs induced most significant down-regulation after 24 hours coculture. Similar to CX3CL1-MSCs, exogenous CX3CL1 treatment could also suppress the expression of TNF-α and IL-1β. We found no statistically significant difference among ISHR-activated group, FB-cocultured group and anti-CX3CL1-MSCs-cocultured group. Soluble CX3CL1 mimics the effect of CX3CL1-MSCs on the expression of TNF-α and IL-1β. MSCs coculture could increase protein expressions of CNTF, BDNF and CX3CR1, which was higher in CX3CL1-MSCs group than that in MSCs group or CX3CL1 group (B). A significant difference was observed between MSCs-treated and CX3CL1-MSCs-treated groups. Anti-CX3CL1-MSCs reverted the upregulation in the expression of CNTF, BDNF and CX3CR1. The changes of CX3CR1 expression on activated microglia was accompanied with the changes of CX3CL1 expression on MSCs. The expression levels of the cytokines were normalized to GAPDH levels. Values are mean ± SD. n = 6, *P < 0.05 Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; FB, Fibroblasts; CX3CL1, exogenous soluble CX3CL1.

    Journal: Ocular immunology and inflammation

    Article Title: Mesenchymal Stem Cells Modulate Light-induced Activation of Retinal Microglia Through CX3CL1/CX3CR1 Signaling.

    doi: 10.3109/09273948.2015.1071405

    Figure Lengend Snippet: FIGURE 3. MSCs coculture affects the protein expression of cytokines by activated microglia. Western blot analyses showed that cocultured with MSCs inhibit the expression of TNF-α and IL-1β by activated microglia (A). Notably, CX3CL1-MSCs induced most significant down-regulation after 24 hours coculture. Similar to CX3CL1-MSCs, exogenous CX3CL1 treatment could also suppress the expression of TNF-α and IL-1β. We found no statistically significant difference among ISHR-activated group, FB-cocultured group and anti-CX3CL1-MSCs-cocultured group. Soluble CX3CL1 mimics the effect of CX3CL1-MSCs on the expression of TNF-α and IL-1β. MSCs coculture could increase protein expressions of CNTF, BDNF and CX3CR1, which was higher in CX3CL1-MSCs group than that in MSCs group or CX3CL1 group (B). A significant difference was observed between MSCs-treated and CX3CL1-MSCs-treated groups. Anti-CX3CL1-MSCs reverted the upregulation in the expression of CNTF, BDNF and CX3CR1. The changes of CX3CR1 expression on activated microglia was accompanied with the changes of CX3CL1 expression on MSCs. The expression levels of the cytokines were normalized to GAPDH levels. Values are mean ± SD. n = 6, *P < 0.05 Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; FB, Fibroblasts; CX3CL1, exogenous soluble CX3CL1.

    Article Snippet: The rat recombinant soluble CX3CL1 protein (5 ng/mL, R&D, USA) was directly added to microglia culture upon ISHR stimulation for 24 h, and the protein expression of CNTF, BDNF, CX3CR1, IL-1β, and TNF-α was detected by Western blot.

    Techniques: Expressing, Western Blot

    FIGURE 5. MSCs coculture suppresses the migratory function of activated microglia. The microglial chemotaxis assay was performed with a chemotaxis apparatus that separated by polycarbonate membrane containing 8-mm pores. The cells were allowed to migrate through the pores, the ones that had migrated to the underside of the membrane were stained with crystal violet (blue) and counted. Cocultured with MSCs inhibited microglial migration, and activated microglia exposed to CX3CL1-MSCs exerted the minimum chemoattractive effect on microglia. There was a significant increase of microglial migration when cocultured with anti-CX3CL1-MSCs. Compared to ISHR-stimulated group, soluble CX3CL1 induced stronger migratory activity of microglia. Scale bars indicate 100μm.Values are mean ± SD. n = 8, *P < 0.05. Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over- expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Journal: Ocular immunology and inflammation

    Article Title: Mesenchymal Stem Cells Modulate Light-induced Activation of Retinal Microglia Through CX3CL1/CX3CR1 Signaling.

    doi: 10.3109/09273948.2015.1071405

    Figure Lengend Snippet: FIGURE 5. MSCs coculture suppresses the migratory function of activated microglia. The microglial chemotaxis assay was performed with a chemotaxis apparatus that separated by polycarbonate membrane containing 8-mm pores. The cells were allowed to migrate through the pores, the ones that had migrated to the underside of the membrane were stained with crystal violet (blue) and counted. Cocultured with MSCs inhibited microglial migration, and activated microglia exposed to CX3CL1-MSCs exerted the minimum chemoattractive effect on microglia. There was a significant increase of microglial migration when cocultured with anti-CX3CL1-MSCs. Compared to ISHR-stimulated group, soluble CX3CL1 induced stronger migratory activity of microglia. Scale bars indicate 100μm.Values are mean ± SD. n = 8, *P < 0.05. Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over- expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Article Snippet: The rat recombinant soluble CX3CL1 protein (5 ng/mL, R&D, USA) was directly added to microglia culture upon ISHR stimulation for 24 h, and the protein expression of CNTF, BDNF, CX3CR1, IL-1β, and TNF-α was detected by Western blot.

    Techniques: Chemotaxis Assay, Membrane, Staining, Migration, Activity Assay, Expressing

    FIGURE 4. MSCs coculture inhibits the proliferation of activated microglia. All cell nuclei stained by Hoechst 33342 showed blue fluorescence, and EdU labeling showed red fluorescence manifesting replicating cells. MSCs coculture inhibited microglial proliferation in vitro. Notably, the percentage of EdU-labelled cells in CX3CL1-MSCs group was lower than that in MSCs group. Accordingly, anti- CX3CL1-MSCs reverted this anti-proliferative effect. There was no significant difference between soluble CX3CL1 group and CX3CL1- MSCs group. Scale bars indicate 100μm. All experiments were done in triplicate, and three independent repeating experiments were performed. Scale bars indicate 100μm. Values are mean ± SD.*P < 0.05. Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Journal: Ocular immunology and inflammation

    Article Title: Mesenchymal Stem Cells Modulate Light-induced Activation of Retinal Microglia Through CX3CL1/CX3CR1 Signaling.

    doi: 10.3109/09273948.2015.1071405

    Figure Lengend Snippet: FIGURE 4. MSCs coculture inhibits the proliferation of activated microglia. All cell nuclei stained by Hoechst 33342 showed blue fluorescence, and EdU labeling showed red fluorescence manifesting replicating cells. MSCs coculture inhibited microglial proliferation in vitro. Notably, the percentage of EdU-labelled cells in CX3CL1-MSCs group was lower than that in MSCs group. Accordingly, anti- CX3CL1-MSCs reverted this anti-proliferative effect. There was no significant difference between soluble CX3CL1 group and CX3CL1- MSCs group. Scale bars indicate 100μm. All experiments were done in triplicate, and three independent repeating experiments were performed. Scale bars indicate 100μm. Values are mean ± SD.*P < 0.05. Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Article Snippet: The rat recombinant soluble CX3CL1 protein (5 ng/mL, R&D, USA) was directly added to microglia culture upon ISHR stimulation for 24 h, and the protein expression of CNTF, BDNF, CX3CR1, IL-1β, and TNF-α was detected by Western blot.

    Techniques: Staining, Labeling, In Vitro, Expressing

    FIGURE 6. MSCs coculture improves the phagocytic capability of activated microglia. Mean fluorescence intensities (MFI) were measured to assess the phagocytic capability of microglia after fluorescent microparticles engulfment. MSCs enhanced the phagocytosis of stimulated microglia. After exposing to CX3CL1-MSCs, microglia phagocytized much more fluorescent microparticles as compared with other groups. Conversely, anti-CX3CL1-MSCs resulted in an inhibition of the phagocytic function. No significant difference was observed between CX3CL1-MSCs group and soluble CX3CL1 group. Unstimulated microglia without microparticles were set as negative control. Results are shown as mean ± SD of at least three independent experiments. *P < 0.05 Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Journal: Ocular immunology and inflammation

    Article Title: Mesenchymal Stem Cells Modulate Light-induced Activation of Retinal Microglia Through CX3CL1/CX3CR1 Signaling.

    doi: 10.3109/09273948.2015.1071405

    Figure Lengend Snippet: FIGURE 6. MSCs coculture improves the phagocytic capability of activated microglia. Mean fluorescence intensities (MFI) were measured to assess the phagocytic capability of microglia after fluorescent microparticles engulfment. MSCs enhanced the phagocytosis of stimulated microglia. After exposing to CX3CL1-MSCs, microglia phagocytized much more fluorescent microparticles as compared with other groups. Conversely, anti-CX3CL1-MSCs resulted in an inhibition of the phagocytic function. No significant difference was observed between CX3CL1-MSCs group and soluble CX3CL1 group. Unstimulated microglia without microparticles were set as negative control. Results are shown as mean ± SD of at least three independent experiments. *P < 0.05 Abbreviations: ISHR, supernatants of homogenized retina were harvested from light-damaged SD rats; CX3CL1-MSCs, CX3CL1 over-expressing MSCs; anti-CX3CL1-MSCs, CX3CL1 blockage on MSCs by a neutralizing antibody; CX3CL1, exogenous soluble CX3CL1.

    Article Snippet: The rat recombinant soluble CX3CL1 protein (5 ng/mL, R&D, USA) was directly added to microglia culture upon ISHR stimulation for 24 h, and the protein expression of CNTF, BDNF, CX3CR1, IL-1β, and TNF-α was detected by Western blot.

    Techniques: Inhibition, Negative Control, Expressing

    Percent of dead CD14+ monocytes elicited by serum starvation in the presence or absence of 100 nM of soluble or full-length CX3CL1 in CX3CR1-WT/WT monocytes. Monocytes cultured in serum-containing media were assayed as control. n = 6. ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using 1-way ANOVA with Tukey’s multiple comparisons test. Data represent the mean ± SEM.

    Journal: JCI Insight

    Article Title: The homozygous CX3CR1-M280 mutation impairs human monocyte survival

    doi: 10.1172/jci.insight.95417

    Figure Lengend Snippet: Percent of dead CD14+ monocytes elicited by serum starvation in the presence or absence of 100 nM of soluble or full-length CX3CL1 in CX3CR1-WT/WT monocytes. Monocytes cultured in serum-containing media were assayed as control. n = 6. ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using 1-way ANOVA with Tukey’s multiple comparisons test. Data represent the mean ± SEM.

    Article Snippet: Recombinant human soluble CX3CL1 (R&D Systems, catalog 362-CX) was then added at a final concentration of 100 nM for 3, 10, or 30 minutes.

    Techniques: Cell Culture, Control

    (A) Representative FACS histograms of propidium iodine (PI) staining in CX3CR1-WT/WT (upper panels) and CX3CR1-M280/M280 (lower panels) CD14+ monocytes following serum starvation in the presence or absence of 100 nM of CX3CL1. (B) Percent of dead CD14+ monocytes elicited by serum starvation in the presence or absence of 100 nM of CX3CL1 in CX3CR1-WT/WT (left panel), CX3CR1-WT/M280 (middle panel), and CX3CR1-M280/M280 (right panel) cells. Shown are paired experimental results with or without CX3CL1. (C) The percent decrease in cell death conferred by CX3CL1 exposure in serum-starved CD14+ monocytes is greater in CX3CR1-WT/WT compared with CX3CR1-WT/M280 cells, while no CX3CL1-induced decrease in cell death is seen in CX3CR1-M280/M280 cells. n = 22 CX3CR1-WT/WT, 11 CX3CR1-WT/M280 and 6 CX3CR1-M280/M280. *P < 0.05; ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using paired 2-tailed t tests (B) or 1-way ANOVA with Tukey’s multiple comparisons test (C). Quantitative data represent the mean ± SEM.

    Journal: JCI Insight

    Article Title: The homozygous CX3CR1-M280 mutation impairs human monocyte survival

    doi: 10.1172/jci.insight.95417

    Figure Lengend Snippet: (A) Representative FACS histograms of propidium iodine (PI) staining in CX3CR1-WT/WT (upper panels) and CX3CR1-M280/M280 (lower panels) CD14+ monocytes following serum starvation in the presence or absence of 100 nM of CX3CL1. (B) Percent of dead CD14+ monocytes elicited by serum starvation in the presence or absence of 100 nM of CX3CL1 in CX3CR1-WT/WT (left panel), CX3CR1-WT/M280 (middle panel), and CX3CR1-M280/M280 (right panel) cells. Shown are paired experimental results with or without CX3CL1. (C) The percent decrease in cell death conferred by CX3CL1 exposure in serum-starved CD14+ monocytes is greater in CX3CR1-WT/WT compared with CX3CR1-WT/M280 cells, while no CX3CL1-induced decrease in cell death is seen in CX3CR1-M280/M280 cells. n = 22 CX3CR1-WT/WT, 11 CX3CR1-WT/M280 and 6 CX3CR1-M280/M280. *P < 0.05; ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using paired 2-tailed t tests (B) or 1-way ANOVA with Tukey’s multiple comparisons test (C). Quantitative data represent the mean ± SEM.

    Article Snippet: Recombinant human soluble CX3CL1 (R&D Systems, catalog 362-CX) was then added at a final concentration of 100 nM for 3, 10, or 30 minutes.

    Techniques: Staining

    Shown are percent of dead monocytes elicited by serum starvation in the presence or absence of 100 nM of CX3CL1 after exposure to 50 μM of the PI3K inhibitor LY294002 (A, n = 5) or 20 μM of the MEK inhibitor PD98059 (B, n = 6), or 100 nM of the PI3K inhibitor wortmannin (C, n = 6) or 20 μM of the MEK inhibitor U0126 (D, n = 5). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using 1-way ANOVA with Tukey’s multiple comparisons test. Data represent the mean ± SEM.

    Journal: JCI Insight

    Article Title: The homozygous CX3CR1-M280 mutation impairs human monocyte survival

    doi: 10.1172/jci.insight.95417

    Figure Lengend Snippet: Shown are percent of dead monocytes elicited by serum starvation in the presence or absence of 100 nM of CX3CL1 after exposure to 50 μM of the PI3K inhibitor LY294002 (A, n = 5) or 20 μM of the MEK inhibitor PD98059 (B, n = 6), or 100 nM of the PI3K inhibitor wortmannin (C, n = 6) or 20 μM of the MEK inhibitor U0126 (D, n = 5). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Statistical analysis was performed using 1-way ANOVA with Tukey’s multiple comparisons test. Data represent the mean ± SEM.

    Article Snippet: Recombinant human soluble CX3CL1 (R&D Systems, catalog 362-CX) was then added at a final concentration of 100 nM for 3, 10, or 30 minutes.

    Techniques: