Review

mouse pf4 elisa kit (Elabscience Biotechnology)

Elabscience Biotechnology is a verified supplier

Elabscience Biotechnology manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Elabscience Biotechnology mouse pf4 elisa kit

TLR8 agonist activates <t>PF4-CXCR3</t> pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Mouse Pf4 Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+pf4+elisa+kit/pmc12901762-237-8-12?v=Elabscience+Biotechnology
Average 94 stars, based on 5 article reviews

mouse pf4 elisa kit - by Bioz Stars, 2026-07

94/100 stars

Images

1) Product Images from "TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms"

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-026-04329-8

TLR8 agonist activates PF4-CXCR3 pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Figure Legend Snippet: TLR8 agonist activates PF4-CXCR3 pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Techniques Used: Control, Marker, Expressing, Gene Expression, Quantitative Proteomics

TLR8 agonist induces PF4 expression through NF-κB signaling pathway. A , B qRT-PCR analysis of Pf4 expression in mouse and human macrophages in the motolimod-treated and control groups ( n = 3). C , D Luminescence assay showing NF-κB pathway activation in mouse and human macrophages following motolimod stimulation ( n = 3). E , F qRT-PCR analysis of Rela expression in Rela -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). G , H Western blotting showing p65 protein levels in RELA -knockdown and control mouse and human macrophages with or without motolimod treatment. I , J qRT-PCR analysis of Pf4 / PF4 expression in Rela / RELA -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). K ELISA quantification of Pf4 levels in the culture supernatant from Rela -knockdown and control mouse macrophages with or without motolimod treatment ( n = 3). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Figure Legend Snippet: TLR8 agonist induces PF4 expression through NF-κB signaling pathway. A , B qRT-PCR analysis of Pf4 expression in mouse and human macrophages in the motolimod-treated and control groups ( n = 3). C , D Luminescence assay showing NF-κB pathway activation in mouse and human macrophages following motolimod stimulation ( n = 3). E , F qRT-PCR analysis of Rela expression in Rela -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). G , H Western blotting showing p65 protein levels in RELA -knockdown and control mouse and human macrophages with or without motolimod treatment. I , J qRT-PCR analysis of Pf4 / PF4 expression in Rela / RELA -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). K ELISA quantification of Pf4 levels in the culture supernatant from Rela -knockdown and control mouse macrophages with or without motolimod treatment ( n = 3). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Techniques Used: Expressing, Quantitative RT-PCR, Control, Luminescence Assay, Activation Assay, Knockdown, Western Blot, Enzyme-linked Immunosorbent Assay

PF4 remodels the TIME and suppresses tumor growth. A , B Tumor growth curves and terminal tumor weights in C57BL/6 mice bearing AKR or MC38 tumors with or without Pf4 overexpression, treated with or without motolimod administered every three days ( n = 6). C Percentage of CD45 + cells among live cells in AKR and MC38 tumor models ( n = 6). D Percentage of cCD4 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). E Percentage of CD8 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). F Percentage of Tregs within the CD45 + population in AKR and MC38 tumor models ( n = 6). G Ratios of cCD4 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). H Ratios of CD8 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). I Representative immunofluorescence staining of CD8α (red) and DAPI (blue) in MC38-Vector or MC38-Pf4-OE tumor sections with or without motolimod treatment. Scale bar: 50 μm. J Quantification of CD8α + positive cell ratio (%) relative to total DAPI + nucleated cells per section ( n = 6). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Figure Legend Snippet: PF4 remodels the TIME and suppresses tumor growth. A , B Tumor growth curves and terminal tumor weights in C57BL/6 mice bearing AKR or MC38 tumors with or without Pf4 overexpression, treated with or without motolimod administered every three days ( n = 6). C Percentage of CD45 + cells among live cells in AKR and MC38 tumor models ( n = 6). D Percentage of cCD4 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). E Percentage of CD8 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). F Percentage of Tregs within the CD45 + population in AKR and MC38 tumor models ( n = 6). G Ratios of cCD4 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). H Ratios of CD8 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). I Representative immunofluorescence staining of CD8α (red) and DAPI (blue) in MC38-Vector or MC38-Pf4-OE tumor sections with or without motolimod treatment. Scale bar: 50 μm. J Quantification of CD8α + positive cell ratio (%) relative to total DAPI + nucleated cells per section ( n = 6). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Techniques Used: Over Expression, Immunofluorescence, Staining, Plasmid Preparation

Image Search Results

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: TLR8 agonist activates PF4-CXCR3 pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Article Snippet: Pf4 levels in culture supernatants were quantified using Mouse PF4 ELISA Kit (Elabscience, #E-EL-M3080) according to the manufacturer’s instructions.

Techniques: Control, Marker, Expressing, Gene Expression, Quantitative Proteomics

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: TLR8 agonist induces PF4 expression through NF-κB signaling pathway. A , B qRT-PCR analysis of Pf4 expression in mouse and human macrophages in the motolimod-treated and control groups ( n = 3). C , D Luminescence assay showing NF-κB pathway activation in mouse and human macrophages following motolimod stimulation ( n = 3). E , F qRT-PCR analysis of Rela expression in Rela -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). G , H Western blotting showing p65 protein levels in RELA -knockdown and control mouse and human macrophages with or without motolimod treatment. I , J qRT-PCR analysis of Pf4 / PF4 expression in Rela / RELA -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). K ELISA quantification of Pf4 levels in the culture supernatant from Rela -knockdown and control mouse macrophages with or without motolimod treatment ( n = 3). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Article Snippet: Pf4 levels in culture supernatants were quantified using Mouse PF4 ELISA Kit (Elabscience, #E-EL-M3080) according to the manufacturer’s instructions.

Techniques: Expressing, Quantitative RT-PCR, Control, Luminescence Assay, Activation Assay, Knockdown, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: PF4 remodels the TIME and suppresses tumor growth. A , B Tumor growth curves and terminal tumor weights in C57BL/6 mice bearing AKR or MC38 tumors with or without Pf4 overexpression, treated with or without motolimod administered every three days ( n = 6). C Percentage of CD45 + cells among live cells in AKR and MC38 tumor models ( n = 6). D Percentage of cCD4 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). E Percentage of CD8 + T cells within the CD45 + population in AKR and MC38 tumor models ( n = 6). F Percentage of Tregs within the CD45 + population in AKR and MC38 tumor models ( n = 6). G Ratios of cCD4 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). H Ratios of CD8 + T cells to Tregs in AKR and MC38 tumor models ( n = 6). I Representative immunofluorescence staining of CD8α (red) and DAPI (blue) in MC38-Vector or MC38-Pf4-OE tumor sections with or without motolimod treatment. Scale bar: 50 μm. J Quantification of CD8α + positive cell ratio (%) relative to total DAPI + nucleated cells per section ( n = 6). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Article Snippet: Pf4 levels in culture supernatants were quantified using Mouse PF4 ELISA Kit (Elabscience, #E-EL-M3080) according to the manufacturer’s instructions.

Techniques: Over Expression, Immunofluorescence, Staining, Plasmid Preparation

(A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).

Journal: bioRxiv

Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

doi: 10.64898/2026.01.12.699090

Figure Lengend Snippet: (A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).

Article Snippet: CXCL4 concentrations were measured in plasma samples using a mouse CXCL4 (platelet factor 4) Quantikine ELISA kit (R&D Systems, MCX400) according to the manufacturer’s instructions.

Techniques: Immunofluorescence, Staining, Confocal Microscopy, Expressing, Ex Vivo, Fluorescence, Activation Assay, Clinical Proteomics, In Vitro, Incubation, Recombinant, Control, Two Tailed Test, Flow Cytometry

Fig. 1 M4 macrophages are activated and CXCL4 is upregulated in BPD. (A) Representative images of H&E staining (arrow represented the pathological structural change in the lung tissues of mice) and IF for F4/80 (a macrophage marker), S100A8, MMP7, and DAPI in lung tissues from NOX (21% O2) and HYX (95% O2) groups (n = 6). (B) Flow cytometric analysis showing the percentage of F4/80+S100A8+MMP7+ cells in NOX and HYX groups (n = 6). (C-D) qRT-PCR analysis and ELISA quantification of CXCL4 expression levels (n = 6). (E) IF staining for F4/80 and CXCL4 in lung tissues (n = 6). (F-G) Western blot analysis of CXCL4, TNF-α, IL-6, MMP7, S100A8, and GAPDH in lung tissues from NOX and HYX groups (n = 6)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 1 M4 macrophages are activated and CXCL4 is upregulated in BPD. (A) Representative images of H&E staining (arrow represented the pathological structural change in the lung tissues of mice) and IF for F4/80 (a macrophage marker), S100A8, MMP7, and DAPI in lung tissues from NOX (21% O2) and HYX (95% O2) groups (n = 6). (B) Flow cytometric analysis showing the percentage of F4/80+S100A8+MMP7+ cells in NOX and HYX groups (n = 6). (C-D) qRT-PCR analysis and ELISA quantification of CXCL4 expression levels (n = 6). (E) IF staining for F4/80 and CXCL4 in lung tissues (n = 6). (F-G) Western blot analysis of CXCL4, TNF-α, IL-6, MMP7, S100A8, and GAPDH in lung tissues from NOX and HYX groups (n = 6)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: Staining, Marker, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

Fig. 2 Loss of CXCL 4 alleviates hyperoxia-induced alveolar epithelial type 2 cells (AT2) injury and suppresses S1P metabolism. (A) H&E staining of lung tissues from WT and CXCL4 KO mice exposed to NOX (21% O2) and HYX (95% O2) conditions for 7 days (n = 6). (B) Quantification of the average surface area of a single alveolus (µm²) (n = 6). (C) Radial Alveolar Count (RAC) analysis (n = 6). (D) Representative images of TUNEL staining (green), SFTPC (red), and DAPI (blue) in lung sections, indicating apoptosis and AT2 cell distribution (n = 6). (E) Quantification of TUNEL-positive cells (n = 6). (F) Quantification of SFTPC + cells per field of view (n = 6). (G-H) Western blot analysis of SPHK1, SPHK2, SPT2, and S1PL, genes associated with sphingosine-1-phosphate metabolism (n = 6)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 2 Loss of CXCL 4 alleviates hyperoxia-induced alveolar epithelial type 2 cells (AT2) injury and suppresses S1P metabolism. (A) H&E staining of lung tissues from WT and CXCL4 KO mice exposed to NOX (21% O2) and HYX (95% O2) conditions for 7 days (n = 6). (B) Quantification of the average surface area of a single alveolus (µm²) (n = 6). (C) Radial Alveolar Count (RAC) analysis (n = 6). (D) Representative images of TUNEL staining (green), SFTPC (red), and DAPI (blue) in lung sections, indicating apoptosis and AT2 cell distribution (n = 6). (E) Quantification of TUNEL-positive cells (n = 6). (F) Quantification of SFTPC + cells per field of view (n = 6). (G-H) Western blot analysis of SPHK1, SPHK2, SPT2, and S1PL, genes associated with sphingosine-1-phosphate metabolism (n = 6)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: Staining, TUNEL Assay, Western Blot

Fig. 3 Deletion of CXCL4 weakens fibrotic lung remodeling. (A) Representative images of lung tissue sections from WT and CXCL4 KO mice under NOX (21% O2) and HYX (95% O2) conditions (n = 6). (B) Measurement of septal thickness (µm) in the NOX_WT, NOX_CXCL4 KO, HYX_WT, and HYX_CXCL4 KO groups (n = 6). (C) Analysis of elastic fibers relative to lung tissue (n = 6). (D) Sirius Red staining showing changes in collagen content (n = 6). (E) Quan tification of collagen amount relative to lung tissue (n = 6). (F) Western blot analysis of phosphorylated SMAD2 (n = 6). (G) Relative expression levels of p-SMAD2/SMAD2 protein ratio (n = 6)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 3 Deletion of CXCL4 weakens fibrotic lung remodeling. (A) Representative images of lung tissue sections from WT and CXCL4 KO mice under NOX (21% O2) and HYX (95% O2) conditions (n = 6). (B) Measurement of septal thickness (µm) in the NOX_WT, NOX_CXCL4 KO, HYX_WT, and HYX_CXCL4 KO groups (n = 6). (C) Analysis of elastic fibers relative to lung tissue (n = 6). (D) Sirius Red staining showing changes in collagen content (n = 6). (E) Quan tification of collagen amount relative to lung tissue (n = 6). (F) Western blot analysis of phosphorylated SMAD2 (n = 6). (G) Relative expression levels of p-SMAD2/SMAD2 protein ratio (n = 6)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: Staining, Western Blot, Expressing

Fig. 4 Deletion of CXCL4 prevents the progression of M4 macrophages in the lung. (A) IF staining for F4/80, S100A8, and DAPI in lung tissues from WT and CXCL4 KO mice under NOX (21% O2) and HYX (95% O2) conditions (n = 6). (B) IF staining for F4/80, MMP7, and DAPI (n = 6). (C) Flow cytometry analysis quantifying F4/80 + S100A8 + MMP7 + cells (%) (n = 6). (D-E) Western blot analysis of CXCL4, TNF-α, IL-6, MMP7, S100A8, and GAPDH (n = 6)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 4 Deletion of CXCL4 prevents the progression of M4 macrophages in the lung. (A) IF staining for F4/80, S100A8, and DAPI in lung tissues from WT and CXCL4 KO mice under NOX (21% O2) and HYX (95% O2) conditions (n = 6). (B) IF staining for F4/80, MMP7, and DAPI (n = 6). (C) Flow cytometry analysis quantifying F4/80 + S100A8 + MMP7 + cells (%) (n = 6). (D-E) Western blot analysis of CXCL4, TNF-α, IL-6, MMP7, S100A8, and GAPDH (n = 6)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: Staining, Flow Cytometry, Western Blot

Fig. 5 CXCL4 induces M4 macrophages in vitro and drives macrophage migration via CCR 1. (A-B) Expression levels of S100A8 and MMP7 in macro phages treated with M-CSF (M0) and CXCL4 (M4) (n = 3). (C-D) Dose-dependent expression of MMP7 and S100A8 in response to varying concentrations of CXCL4 (4, 2, 1, 0.5 µM) (n = 3). (E) IF staining of S100A8 and DAPI (n = 3). (F) IF staining of MMP7 and DAPI (n = 3). (G-H) ELISA results for MMP7 and S100A8 (n = 3). (I-J) Macrophage migration assay comparing control, CXCL4, CCR1 inhibitor (CCR1 Inhi), and CXCL4 + CCR1 Inhi groups. Arrows represented the type of migrated cells (n = 3)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 5 CXCL4 induces M4 macrophages in vitro and drives macrophage migration via CCR 1. (A-B) Expression levels of S100A8 and MMP7 in macro phages treated with M-CSF (M0) and CXCL4 (M4) (n = 3). (C-D) Dose-dependent expression of MMP7 and S100A8 in response to varying concentrations of CXCL4 (4, 2, 1, 0.5 µM) (n = 3). (E) IF staining of S100A8 and DAPI (n = 3). (F) IF staining of MMP7 and DAPI (n = 3). (G-H) ELISA results for MMP7 and S100A8 (n = 3). (I-J) Macrophage migration assay comparing control, CXCL4, CCR1 inhibitor (CCR1 Inhi), and CXCL4 + CCR1 Inhi groups. Arrows represented the type of migrated cells (n = 3)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: In Vitro, Migration, Expressing, Staining, Enzyme-linked Immunosorbent Assay, Control

Fig. 6 CXCL4 deficiency promotes lung matrix remodeling during regeneration. (A) H&E staining of lung tissues from WT and CXCL4 KO mice exposed to HYX followed by a recovery period under NOX conditions (n = 6). (B) Measurement of the average surface area of a single alveolus (µm²) (n = 6). (C) Radial Alveolar Count (RAC) analysis (n = 6). (D) Measurement of septal thickness (µm) (n = 6). (E-F) Quantification of collagen amount relative to lung tissue (n = 6)

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.

doi: 10.1186/s10020-024-01043-y

Figure Lengend Snippet: Fig. 6 CXCL4 deficiency promotes lung matrix remodeling during regeneration. (A) H&E staining of lung tissues from WT and CXCL4 KO mice exposed to HYX followed by a recovery period under NOX conditions (n = 6). (B) Measurement of the average surface area of a single alveolus (µm²) (n = 6). (C) Radial Alveolar Count (RAC) analysis (n = 6). (D) Measurement of septal thickness (µm) (n = 6). (E-F) Quantification of collagen amount relative to lung tissue (n = 6)

Article Snippet: CXCL4 concentrations were quantified with a mouse CXCL4/PF-4 ELISA kit (MCX400, R&D Systems, USA).

Techniques: Staining

Review

Structured Review

Images

1) Product Images from "TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms"

Similar Products

Image Search Results