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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/result/recombinant soluble fractalkine/product/R&D Systems
    Average 92 stars, based on 5 article reviews
    recombinant soluble fractalkine - by Bioz Stars, 2026-06
    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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    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

    Figure 3. Interactions of CX3CL1 and CX3CR1-positive macrophages increase invasion of breast cancer cells. A and B, Correlation of Cx3cr1 and Cx3cl1 mRNA expression in liver and lung of PDX models and non-tumor bearing mice. C, Comparison of Cx3cl1 mRNA expression in liver and lung tissues of PDX models and non-tumor bearing mice. D, IHC about CX3CL1 in 4T1-tumor bearing mice. E, Identification of CX3CL1-positive endothelial cell population a. Immunofluorescence staining against CX3CL1 (green) and F4/80 (red) in liver tissues of non-tumor bearing mouse and 4T1 bearing mouse. co-localized areas were shown as white color. F, Real time PCR of Cx3cl1 in 4T1-tumor bearing mice. G, Trans-well migration assay of Raw264.7 cell line with or without CX3CL1. H, Trans-well invasion assay of siNTC or siCX3CR1 treated Raw264.7 cell line with or without CX3CL1. I, Trans-well invasion assay of 4T1 and EO771 breast cancer cell lines in matrigel pre-conditioned by CX3CL1 and CX3CR1 inhibitor AZD8797 treated Raw264.7 conditioned media. Error bars denote mean SD. , P < 0.05; , P <0.01; , P < 0.001. P values are determined by the Mann–Whitney test.

    Journal: Molecular Cancer Research

    Article Title: Triple-Negative Breast Cancer-Derived Extracellular Vesicles Promote a Hepatic Premetastatic Niche via a Cascade of Microenvironment Remodeling

    doi: 10.1158/1541-7786.mcr-22-0673

    Figure Lengend Snippet: Figure 3. Interactions of CX3CL1 and CX3CR1-positive macrophages increase invasion of breast cancer cells. A and B, Correlation of Cx3cr1 and Cx3cl1 mRNA expression in liver and lung of PDX models and non-tumor bearing mice. C, Comparison of Cx3cl1 mRNA expression in liver and lung tissues of PDX models and non-tumor bearing mice. D, IHC about CX3CL1 in 4T1-tumor bearing mice. E, Identification of CX3CL1-positive endothelial cell population a. Immunofluorescence staining against CX3CL1 (green) and F4/80 (red) in liver tissues of non-tumor bearing mouse and 4T1 bearing mouse. co-localized areas were shown as white color. F, Real time PCR of Cx3cl1 in 4T1-tumor bearing mice. G, Trans-well migration assay of Raw264.7 cell line with or without CX3CL1. H, Trans-well invasion assay of siNTC or siCX3CR1 treated Raw264.7 cell line with or without CX3CL1. I, Trans-well invasion assay of 4T1 and EO771 breast cancer cell lines in matrigel pre-conditioned by CX3CL1 and CX3CR1 inhibitor AZD8797 treated Raw264.7 conditioned media. Error bars denote mean SD. , P < 0.05; , P <0.01; , P < 0.001. P values are determined by the Mann–Whitney test.

    Article Snippet: The soluble CX3CL1 ELISA was performed with filtered plasma samples of total 155 patients with breast cancer which were composed of 59 metastasis patients and 96 non-metastasis patients by Human CX3CL1/Fractalkine Quantikine ELISA Kit (R&D Systems).

    Techniques: Expressing, Comparison, Staining, Real-time Polymerase Chain Reaction, Migration, Invasion Assay, MANN-WHITNEY

    Figure 4. Interactions of CX3CL1 and CX3CR1-positive macrophages increase ECM remodeling by regulation of MMP9 expression. A, Comparison of Mmp9 mRNA expression in liver and lung tissues of PDX models and non-tumor bearing mice. B, Western blot results showing regulation of MMP9 expression in Raw264.7 cell line by CX3CL1 treatment with or without CX3CR1 knockdown (top) or AZD8797 (bottom). C, Trans-well invasion assay of Raw264.7 cell line with or without CX3CL1 and MMP9 inhibitor JNJ0966. D, Trans-well invasion assay of 4T1 breast cancer cell lines in matrigel pre-conditioned by CX3CL1 and JNJ0966 treated Raw264.7 conditioned media. E, Tube formation assay of HUVEC cells in matrigel pre-conditioned by CX3CL1 and AZD8797 treated Raw264.7 conditioned media (arrow: well formed endothelial tube. F, Tube formation assay of HUVEC cells in matrigel pre-conditioned by CX3CL1 and JNJ0966 treated Raw264.7 conditioned media (arrow: well formed endothelial tube). Error bars denote mean SD. , P < 0.05; , P < 0.001. P values are determined by the Mann–Whitney test.

    Journal: Molecular Cancer Research

    Article Title: Triple-Negative Breast Cancer-Derived Extracellular Vesicles Promote a Hepatic Premetastatic Niche via a Cascade of Microenvironment Remodeling

    doi: 10.1158/1541-7786.mcr-22-0673

    Figure Lengend Snippet: Figure 4. Interactions of CX3CL1 and CX3CR1-positive macrophages increase ECM remodeling by regulation of MMP9 expression. A, Comparison of Mmp9 mRNA expression in liver and lung tissues of PDX models and non-tumor bearing mice. B, Western blot results showing regulation of MMP9 expression in Raw264.7 cell line by CX3CL1 treatment with or without CX3CR1 knockdown (top) or AZD8797 (bottom). C, Trans-well invasion assay of Raw264.7 cell line with or without CX3CL1 and MMP9 inhibitor JNJ0966. D, Trans-well invasion assay of 4T1 breast cancer cell lines in matrigel pre-conditioned by CX3CL1 and JNJ0966 treated Raw264.7 conditioned media. E, Tube formation assay of HUVEC cells in matrigel pre-conditioned by CX3CL1 and AZD8797 treated Raw264.7 conditioned media (arrow: well formed endothelial tube. F, Tube formation assay of HUVEC cells in matrigel pre-conditioned by CX3CL1 and JNJ0966 treated Raw264.7 conditioned media (arrow: well formed endothelial tube). Error bars denote mean SD. , P < 0.05; , P < 0.001. P values are determined by the Mann–Whitney test.

    Article Snippet: The soluble CX3CL1 ELISA was performed with filtered plasma samples of total 155 patients with breast cancer which were composed of 59 metastasis patients and 96 non-metastasis patients by Human CX3CL1/Fractalkine Quantikine ELISA Kit (R&D Systems).

    Techniques: Expressing, Comparison, Western Blot, Knockdown, Invasion Assay, Tube Formation Assay, MANN-WHITNEY

    Figure 7. CX3CL1 levels in plasma of patients with breast cancer indicates future development of liver metastasis. A, Soluble CX3CL1 levels in plasma of 96 non-metastasis or 59 distant metastasis breast cancer patients identified by ELISA. B, Comparison of Kaplan-Meier distant metastasis free survival curves according to CX3CL1 levels in plasma of patients with breast cancer (HR; Hazard ratio, CI; Confidence interval). C, Summary of our experimental results. Error bars denote mean SD. , P < 0.05; , P < 0.001. P values are determined by the Mann–Whitney test for A and log rank test for B.

    Journal: Molecular Cancer Research

    Article Title: Triple-Negative Breast Cancer-Derived Extracellular Vesicles Promote a Hepatic Premetastatic Niche via a Cascade of Microenvironment Remodeling

    doi: 10.1158/1541-7786.mcr-22-0673

    Figure Lengend Snippet: Figure 7. CX3CL1 levels in plasma of patients with breast cancer indicates future development of liver metastasis. A, Soluble CX3CL1 levels in plasma of 96 non-metastasis or 59 distant metastasis breast cancer patients identified by ELISA. B, Comparison of Kaplan-Meier distant metastasis free survival curves according to CX3CL1 levels in plasma of patients with breast cancer (HR; Hazard ratio, CI; Confidence interval). C, Summary of our experimental results. Error bars denote mean SD. , P < 0.05; , P < 0.001. P values are determined by the Mann–Whitney test for A and log rank test for B.

    Article Snippet: The soluble CX3CL1 ELISA was performed with filtered plasma samples of total 155 patients with breast cancer which were composed of 59 metastasis patients and 96 non-metastasis patients by Human CX3CL1/Fractalkine Quantikine ELISA Kit (R&D Systems).

    Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Comparison, MANN-WHITNEY

    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