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apc cyanine 7 anti mouse cx3cr1 (Revvity Signals)

Name: apc cyanine 7 anti mouse cx3cr1
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Rating: 86 (1 reviews)

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Revvity Signals apc cyanine 7 anti mouse cx3cr1

FSTL1 facilitates stem cell-mediated Ly6C − <t>CX3CR1</t> + subset remodelling. a UMAP analysis of 4300 macrophages from 3 PBS- and 3 MSC-treated mice identified 15 distinct cell clusters. b Cluster distribution of cells in PBS- (gray) and MSC- (purple) treated mice. c Comparison of the populations of different cell lineages between PBS-treated and MSC-treated livers. d The relative percentages of different cell lineages in each group, coloured according to cell lineage. PBS: n = 3 liver samples from PBS-treated mice; MSC: n = 3 liver samples from MSC-treated mice. e Heatmap displaying the relative expression levels of marker genes in 15 cell lineages (top, colour-coded by cell lineage), with exemplar genes labelled in Cluster 5. The columns denote cells; the rows denote genes. f Marker expression in different clusters. g – j The percentages of the Ly6C − CX3CR1 + subset among the total viable hepatic CD45 + cells and the cell count of the Ly6C − CX3CR1 + subset were normalized to the liver weight, as determined by flow cytometry. g , h The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 6) and WT littermates ( n = 6) at 24 h ( g ) and 48 h ( h ) after MSC infusion. i The Ly6C − CX3CR1 + subset was evaluated in C57BL/6 mice treated with ( n = 5) or without the FSTL1 neutralizing antibody 22B6 ( n = 5) at 48 h after MSC infusion. j The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 5) and WT littermates ( n = 5) at 48 h after MNC infusion. * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by a two-tailed unpaired t -test ( g – j ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Apc Cyanine 7 Anti Mouse Cx3cr1, supplied by Revvity Signals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages"

Article Title: Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages

Journal: Signal Transduction and Targeted Therapy

doi: 10.1038/s41392-025-02162-6

FSTL1 facilitates stem cell-mediated Ly6C − CX3CR1 + subset remodelling. a UMAP analysis of 4300 macrophages from 3 PBS- and 3 MSC-treated mice identified 15 distinct cell clusters. b Cluster distribution of cells in PBS- (gray) and MSC- (purple) treated mice. c Comparison of the populations of different cell lineages between PBS-treated and MSC-treated livers. d The relative percentages of different cell lineages in each group, coloured according to cell lineage. PBS: n = 3 liver samples from PBS-treated mice; MSC: n = 3 liver samples from MSC-treated mice. e Heatmap displaying the relative expression levels of marker genes in 15 cell lineages (top, colour-coded by cell lineage), with exemplar genes labelled in Cluster 5. The columns denote cells; the rows denote genes. f Marker expression in different clusters. g – j The percentages of the Ly6C − CX3CR1 + subset among the total viable hepatic CD45 + cells and the cell count of the Ly6C − CX3CR1 + subset were normalized to the liver weight, as determined by flow cytometry. g , h The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 6) and WT littermates ( n = 6) at 24 h ( g ) and 48 h ( h ) after MSC infusion. i The Ly6C − CX3CR1 + subset was evaluated in C57BL/6 mice treated with ( n = 5) or without the FSTL1 neutralizing antibody 22B6 ( n = 5) at 48 h after MSC infusion. j The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 5) and WT littermates ( n = 5) at 48 h after MNC infusion. * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by a two-tailed unpaired t -test ( g – j ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Figure Legend Snippet: FSTL1 facilitates stem cell-mediated Ly6C − CX3CR1 + subset remodelling. a UMAP analysis of 4300 macrophages from 3 PBS- and 3 MSC-treated mice identified 15 distinct cell clusters. b Cluster distribution of cells in PBS- (gray) and MSC- (purple) treated mice. c Comparison of the populations of different cell lineages between PBS-treated and MSC-treated livers. d The relative percentages of different cell lineages in each group, coloured according to cell lineage. PBS: n = 3 liver samples from PBS-treated mice; MSC: n = 3 liver samples from MSC-treated mice. e Heatmap displaying the relative expression levels of marker genes in 15 cell lineages (top, colour-coded by cell lineage), with exemplar genes labelled in Cluster 5. The columns denote cells; the rows denote genes. f Marker expression in different clusters. g – j The percentages of the Ly6C − CX3CR1 + subset among the total viable hepatic CD45 + cells and the cell count of the Ly6C − CX3CR1 + subset were normalized to the liver weight, as determined by flow cytometry. g , h The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 6) and WT littermates ( n = 6) at 24 h ( g ) and 48 h ( h ) after MSC infusion. i The Ly6C − CX3CR1 + subset was evaluated in C57BL/6 mice treated with ( n = 5) or without the FSTL1 neutralizing antibody 22B6 ( n = 5) at 48 h after MSC infusion. j The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 5) and WT littermates ( n = 5) at 48 h after MNC infusion. * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by a two-tailed unpaired t -test ( g – j ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Techniques Used: Comparison, Expressing, Marker, Cell Counting, Flow Cytometry, Two Tailed Test

Inflammatory macrophages reprogram metabolism and improve the immunosuppressive capacity of MSCs. a Schematic illustration of the hepatic fibrosis model establishment and the MSC-based treatment strategy. b – d The degree of fibrosis was evaluated in the PBS-, MSC-, CsA+MSC-, and PF4136409 + MSC-treated groups at 4 weeks postinfusion ( n = 5). b Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Schematic of the in vitro coculture system for MSCs and BMDMs. f Volcano plot showing genes whose expression changed in MSCs cocultured with BMDMs compared with control MSCs, as determined by RNA-seq ( n = 4). g – j GSEA plots (left) and heatmaps (right) of the RNA-seq data of MSCs cocultured with BMDMs and control MSCs. Representative genes from each category are shown. FDR, false discovery rate; NES, normalized enrichment score. n = 4 mice per group. Statistical significance was determined by linear modelling and Bayesian statistics after correcting for multiple testing with the Benjamini–Hochberg procedure ( f ) or the Wald test with Benjamini–Hochberg’s multiple-comparison correction ( g – j ). k Gene expression was determined by qPCR in MSCs cocultured with increasing amounts of BMDMs ( n = 4). l Schematic of the in vitro coculture system for MSCs and BMDMs. m Gene expression was determined by qPCR in altered amounts of BMDMs cocultured with MSCs ( n = 4). n , o The percentages of the Ly6C − CX3CR1 + subset were determined via flow cytometry in altered amounts of BMDMs after coculture with MSCs ( n = 6). * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( k , m , o ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Figure Legend Snippet: Inflammatory macrophages reprogram metabolism and improve the immunosuppressive capacity of MSCs. a Schematic illustration of the hepatic fibrosis model establishment and the MSC-based treatment strategy. b – d The degree of fibrosis was evaluated in the PBS-, MSC-, CsA+MSC-, and PF4136409 + MSC-treated groups at 4 weeks postinfusion ( n = 5). b Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Schematic of the in vitro coculture system for MSCs and BMDMs. f Volcano plot showing genes whose expression changed in MSCs cocultured with BMDMs compared with control MSCs, as determined by RNA-seq ( n = 4). g – j GSEA plots (left) and heatmaps (right) of the RNA-seq data of MSCs cocultured with BMDMs and control MSCs. Representative genes from each category are shown. FDR, false discovery rate; NES, normalized enrichment score. n = 4 mice per group. Statistical significance was determined by linear modelling and Bayesian statistics after correcting for multiple testing with the Benjamini–Hochberg procedure ( f ) or the Wald test with Benjamini–Hochberg’s multiple-comparison correction ( g – j ). k Gene expression was determined by qPCR in MSCs cocultured with increasing amounts of BMDMs ( n = 4). l Schematic of the in vitro coculture system for MSCs and BMDMs. m Gene expression was determined by qPCR in altered amounts of BMDMs cocultured with MSCs ( n = 4). n , o The percentages of the Ly6C − CX3CR1 + subset were determined via flow cytometry in altered amounts of BMDMs after coculture with MSCs ( n = 6). * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( k , m , o ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Techniques Used: Staining, In Vitro, Expressing, Control, RNA Sequencing, Comparison, Gene Expression, Flow Cytometry

Administration of FSTL1 rescues the defective therapeutic effect of MSCs in Fstl1 +/ − mice. a Schematic illustration of hepatic fibrosis model establishment and the MSC-based early treatment strategy. b The fibrosis degree was evaluated in Fstl1 +/ − mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 4 weeks postinfusion. Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Total liver RNA was extracted and the expression of Col1 and α-Sma was determined by qPCR. f – h Macrophage infiltration was evaluated in Fstl1 +/− mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 48 h post infusion. f The percentages of F4/80 + CD11b + cells among the total number of viable CD45 + cells and the number of CD11b + F4/80 + cells normalized to the liver weight were determined by flow cytometry. ( g ) The percentages of Ly6C − CX3CR1 + cells among the total number of viable CD45 + cells and the cell counts of the Ly6C − CX3CR1 + subset were compared. ( h ) F4/80 + macrophages were sorted from the livers of Fstl1 +/ − mice treated with FSTL1 or FSTL1 + PF4136409 at 24 h post infusion, and the mRNA levels of inflammatory markers ( Arg-1 , iNOS ) and Mmp9 were determined by qPCR. * p < 0.05, ** p < 0.01, and n.s. not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( c , d , f , g ) or two-way ANOVA with Tukey multiple comparison test ( e , h ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Figure Legend Snippet: Administration of FSTL1 rescues the defective therapeutic effect of MSCs in Fstl1 +/ − mice. a Schematic illustration of hepatic fibrosis model establishment and the MSC-based early treatment strategy. b The fibrosis degree was evaluated in Fstl1 +/ − mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 4 weeks postinfusion. Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Total liver RNA was extracted and the expression of Col1 and α-Sma was determined by qPCR. f – h Macrophage infiltration was evaluated in Fstl1 +/− mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 48 h post infusion. f The percentages of F4/80 + CD11b + cells among the total number of viable CD45 + cells and the number of CD11b + F4/80 + cells normalized to the liver weight were determined by flow cytometry. ( g ) The percentages of Ly6C − CX3CR1 + cells among the total number of viable CD45 + cells and the cell counts of the Ly6C − CX3CR1 + subset were compared. ( h ) F4/80 + macrophages were sorted from the livers of Fstl1 +/ − mice treated with FSTL1 or FSTL1 + PF4136409 at 24 h post infusion, and the mRNA levels of inflammatory markers ( Arg-1 , iNOS ) and Mmp9 were determined by qPCR. * p < 0.05, ** p < 0.01, and n.s. not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( c , d , f , g ) or two-way ANOVA with Tukey multiple comparison test ( e , h ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Techniques Used: Staining, Expressing, Flow Cytometry, Comparison

Image Search Results

Co-administration of CX3CL1 and M-CSF enhances centripetal migration and prolonged retention of microglia after SCI. ( A ) Schematic diagram illustrating in situ injection of 2 µl CX3CL1 and M-CSF (CX3CL1 + M-CSF group), 1 µl CX3CL1 (CX3CL1 group), 1 µl M-CSF (M-CSF group) or 1 µl PBS (PBS group) into the epicenter immediately after SCI in WT and CX3CR1 GFP CCR2 RFP mice. Histological analysis was performed at 28 dpi. ( B ) Immunofluorescence staining of GFAP (green) and Fascin-1 (red) showing an augmented presence of Fascin-1 + microglia at the injury sites in the CX3CL1 + M-CSF group compared to the CX3CL1 and M-CSF groups at 28 dpi of WT mice. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. ( C ) Quantification of the number of Fascin-1 + cells in the epicenter at 28 dpi ( n = 4 mice per group). ( D ) Immunofluorescence staining of Mac-2 (red) and DAPI (blue) in sagittal sections from the CX3CL1 + M-CSF, CX3CL1 and M-CSF groups at 28 dpi of WT mice. ( E ) Quantification of the percentage of Mac-2 + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 4 mice per group). ( F ) Representative immunofluorescence images of RFP (red) and GFP (green) in sagittal sections of the injured spinal cord from the CX3CL1 + M-CSF and PBS groups at 28 dpi of CX3CR1 GFP CCR2 RFP mice. ( G ) Quantification of the percentage of RFP + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 3 mice per group). The data are presented as means ± SEM (error bars). **** P < 0.0001, the CX3CL1 + M-CSF group versus the CX3CL1, M-CSF and PBS groups. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc tests ( C and E ), or Student’s two-tailed unpaired t-test ( G ). Scale bars = 100 μm ( B and F ), 200 μm ( D ), 20 μm ( ROI )

Journal: Journal of Neuroinflammation

Article Title: Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair

doi: 10.1186/s12974-025-03411-9

Figure Lengend Snippet: Co-administration of CX3CL1 and M-CSF enhances centripetal migration and prolonged retention of microglia after SCI. ( A ) Schematic diagram illustrating in situ injection of 2 µl CX3CL1 and M-CSF (CX3CL1 + M-CSF group), 1 µl CX3CL1 (CX3CL1 group), 1 µl M-CSF (M-CSF group) or 1 µl PBS (PBS group) into the epicenter immediately after SCI in WT and CX3CR1 GFP CCR2 RFP mice. Histological analysis was performed at 28 dpi. ( B ) Immunofluorescence staining of GFAP (green) and Fascin-1 (red) showing an augmented presence of Fascin-1 + microglia at the injury sites in the CX3CL1 + M-CSF group compared to the CX3CL1 and M-CSF groups at 28 dpi of WT mice. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. ( C ) Quantification of the number of Fascin-1 + cells in the epicenter at 28 dpi ( n = 4 mice per group). ( D ) Immunofluorescence staining of Mac-2 (red) and DAPI (blue) in sagittal sections from the CX3CL1 + M-CSF, CX3CL1 and M-CSF groups at 28 dpi of WT mice. ( E ) Quantification of the percentage of Mac-2 + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 4 mice per group). ( F ) Representative immunofluorescence images of RFP (red) and GFP (green) in sagittal sections of the injured spinal cord from the CX3CL1 + M-CSF and PBS groups at 28 dpi of CX3CR1 GFP CCR2 RFP mice. ( G ) Quantification of the percentage of RFP + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 3 mice per group). The data are presented as means ± SEM (error bars). **** P < 0.0001, the CX3CL1 + M-CSF group versus the CX3CL1, M-CSF and PBS groups. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc tests ( C and E ), or Student’s two-tailed unpaired t-test ( G ). Scale bars = 100 μm ( B and F ), 200 μm ( D ), 20 μm ( ROI )

Article Snippet: The CX3CRl GFP CCR2 RFP mice [ ] and CX3CR1 −/− (CX3CR1 GFP/GFP ) mice [ ] at age of 8 weeks were obtained from Jackson Laboratory (catalog no. 032127 and 005582).

Techniques: Migration, In Situ, Injection, Immunofluorescence, Staining, Two Tailed Test

The beneficial effects of combined administration of CX3CL1 and M-CSF are specifically blocked in CX3CR1 −/− mice. (A) Schematic diagram illustrating in situ injection of 2 µl of CX3CL1 and M-CSF into the epicenter immediately after SCI in CX3CR1 −/− (CX3CR1 GFP/GFP ) and CX3CR1 +/− (CX3CR1 +/GFP ) mice. Histological analysis was performed at 28 dpi. (B) Representative immunofluorescence images of GFAP (red) and GFP (green) from sagittal sections of the injured spinal cord of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. (C) Quantification of the number of GFP + microglia in the epicenter of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (D) Representative images of sections of the injured spinal cord of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi, stained with antibodies against GFAP (green), PDGFRβ (red) and NeuN (purple). (E and F) Quantification of the percentage of GFAP − area (E) and PDGFRβ + area (F) within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (G) Quantification of NeuN + neurons in Z1–Z3 zones adjacent to central lesion core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (H) Immunofluorescence staining of 5-HT (red) and DAPI (blue) in sagittal sections of the injured spinal cord from CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. White arrowheads indicate the lesion site. (I) Quantification of 5-HT density within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. ( n = 3 mice per group). (J) Time course of functional recovery of CXCR1 −/− and CX3CR1 +/− mice assessed by the BMS score after the combined treatment of CX3CL1 and M-CSF post-SCI ( n = 6 mice per group). (K) Footprint analysis performed at 28 dpi reveals improved functional recovery in the CX3CR1 +/− mice after the combined treatment of CX3CL1 and M-CSF. (L) Quantification of the footprint analysis parameters (stride length, stride width, and paw rotation) in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 6 mice per group). The data are presented as means ± SEM (error bars). * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001, the CX3CR1 +/− mice versus the CX3CR1 −/− mice. Statistical analysis was performed using two-way ANOVA (G and J) followed by Bonferroni post hoc tests’, or Student’s two-tailed unpaired t-test ( C , E , F , I and L ). Scale bars = 200 μm ( D and H ), 100 μm ( B ), 20 μm ( ROI )

Journal: Journal of Neuroinflammation

Article Title: Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair

doi: 10.1186/s12974-025-03411-9

Figure Lengend Snippet: The beneficial effects of combined administration of CX3CL1 and M-CSF are specifically blocked in CX3CR1 −/− mice. (A) Schematic diagram illustrating in situ injection of 2 µl of CX3CL1 and M-CSF into the epicenter immediately after SCI in CX3CR1 −/− (CX3CR1 GFP/GFP ) and CX3CR1 +/− (CX3CR1 +/GFP ) mice. Histological analysis was performed at 28 dpi. (B) Representative immunofluorescence images of GFAP (red) and GFP (green) from sagittal sections of the injured spinal cord of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. (C) Quantification of the number of GFP + microglia in the epicenter of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (D) Representative images of sections of the injured spinal cord of CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi, stained with antibodies against GFAP (green), PDGFRβ (red) and NeuN (purple). (E and F) Quantification of the percentage of GFAP − area (E) and PDGFRβ + area (F) within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (G) Quantification of NeuN + neurons in Z1–Z3 zones adjacent to central lesion core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3 mice per group). (H) Immunofluorescence staining of 5-HT (red) and DAPI (blue) in sagittal sections of the injured spinal cord from CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. White arrowheads indicate the lesion site. (I) Quantification of 5-HT density within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. ( n = 3 mice per group). (J) Time course of functional recovery of CXCR1 −/− and CX3CR1 +/− mice assessed by the BMS score after the combined treatment of CX3CL1 and M-CSF post-SCI ( n = 6 mice per group). (K) Footprint analysis performed at 28 dpi reveals improved functional recovery in the CX3CR1 +/− mice after the combined treatment of CX3CL1 and M-CSF. (L) Quantification of the footprint analysis parameters (stride length, stride width, and paw rotation) in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 6 mice per group). The data are presented as means ± SEM (error bars). * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001, the CX3CR1 +/− mice versus the CX3CR1 −/− mice. Statistical analysis was performed using two-way ANOVA (G and J) followed by Bonferroni post hoc tests’, or Student’s two-tailed unpaired t-test ( C , E , F , I and L ). Scale bars = 200 μm ( D and H ), 100 μm ( B ), 20 μm ( ROI )

Article Snippet: The CX3CRl GFP CCR2 RFP mice [ ] and CX3CR1 −/− (CX3CR1 GFP/GFP ) mice [ ] at age of 8 weeks were obtained from Jackson Laboratory (catalog no. 032127 and 005582).

Techniques: In Situ, Injection, Immunofluorescence, Staining, Functional Assay, Two Tailed Test

Co-administration of CX3CL1 and M-CSF may exert beneficial effects by enhancing SYK levels in CX3CR1 + microglia and reducing foamy cell recruitment after SCI. ( A ) Immunofluorescence staining of SYK (green) and DAPI (blue) in sagittal sections from the CX3CL1 + M-CSF, CX3CL1, M-CSF, Control and PBS groups at 28 dpi. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. ( B ) Quantification of the percentage of SYK + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 4 mice per group). ( C ) Lipid accumulation was determined by ORO staining at 28 dpi. ( D ) The quantification of the ratio of the mean density of ORO signal to the lesion area within the spinal cord segment spanning the injured core at 28 dpi ( n = 3 mice per group). ( E ) Representative immunofluorescence images of SYK (red) and GFP (green) in sagittal sections of the injured spinal cord from CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. These mice were treated with an in situ injection of 2 µl of CX3CL1 and M-CSF into the epicenter immediately after SCI. ( F ) Quantification of the percentage of SYK + area within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3). The data are presented as means ± SEM (error bars). * P < 0.05 and ** P < 0.01, *** P < 0.001 and **** P < 0.0001. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc tests ( B and D ), or Student’s two-tailed unpaired t-test ( F ). Scale bars = 200 μm ( A , C and E ), 20 μm ( ROI )

Journal: Journal of Neuroinflammation

Article Title: Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair

doi: 10.1186/s12974-025-03411-9

Figure Lengend Snippet: Co-administration of CX3CL1 and M-CSF may exert beneficial effects by enhancing SYK levels in CX3CR1 + microglia and reducing foamy cell recruitment after SCI. ( A ) Immunofluorescence staining of SYK (green) and DAPI (blue) in sagittal sections from the CX3CL1 + M-CSF, CX3CL1, M-CSF, Control and PBS groups at 28 dpi. ROI represents the high-magnification image within the dotted box on the left. Asterisks show the injured core. ( B ) Quantification of the percentage of SYK + area within the spinal cord segment spanning the injured core at 28 dpi ( n = 4 mice per group). ( C ) Lipid accumulation was determined by ORO staining at 28 dpi. ( D ) The quantification of the ratio of the mean density of ORO signal to the lesion area within the spinal cord segment spanning the injured core at 28 dpi ( n = 3 mice per group). ( E ) Representative immunofluorescence images of SYK (red) and GFP (green) in sagittal sections of the injured spinal cord from CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi. These mice were treated with an in situ injection of 2 µl of CX3CL1 and M-CSF into the epicenter immediately after SCI. ( F ) Quantification of the percentage of SYK + area within the spinal cord segment spanning the injured core in CX3CR1 −/− and CX3CR1 +/− mice at 28 dpi ( n = 3). The data are presented as means ± SEM (error bars). * P < 0.05 and ** P < 0.01, *** P < 0.001 and **** P < 0.0001. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc tests ( B and D ), or Student’s two-tailed unpaired t-test ( F ). Scale bars = 200 μm ( A , C and E ), 20 μm ( ROI )

Article Snippet: The CX3CRl GFP CCR2 RFP mice [ ] and CX3CR1 −/− (CX3CR1 GFP/GFP ) mice [ ] at age of 8 weeks were obtained from Jackson Laboratory (catalog no. 032127 and 005582).

Techniques: Immunofluorescence, Staining, Control, In Situ, Injection, Two Tailed Test

Journal: Signal Transduction and Targeted Therapy

Article Title: Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages

doi: 10.1038/s41392-025-02162-6

Figure Lengend Snippet: FSTL1 facilitates stem cell-mediated Ly6C − CX3CR1 + subset remodelling. a UMAP analysis of 4300 macrophages from 3 PBS- and 3 MSC-treated mice identified 15 distinct cell clusters. b Cluster distribution of cells in PBS- (gray) and MSC- (purple) treated mice. c Comparison of the populations of different cell lineages between PBS-treated and MSC-treated livers. d The relative percentages of different cell lineages in each group, coloured according to cell lineage. PBS: n = 3 liver samples from PBS-treated mice; MSC: n = 3 liver samples from MSC-treated mice. e Heatmap displaying the relative expression levels of marker genes in 15 cell lineages (top, colour-coded by cell lineage), with exemplar genes labelled in Cluster 5. The columns denote cells; the rows denote genes. f Marker expression in different clusters. g – j The percentages of the Ly6C − CX3CR1 + subset among the total viable hepatic CD45 + cells and the cell count of the Ly6C − CX3CR1 + subset were normalized to the liver weight, as determined by flow cytometry. g , h The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 6) and WT littermates ( n = 6) at 24 h ( g ) and 48 h ( h ) after MSC infusion. i The Ly6C − CX3CR1 + subset was evaluated in C57BL/6 mice treated with ( n = 5) or without the FSTL1 neutralizing antibody 22B6 ( n = 5) at 48 h after MSC infusion. j The Ly6C − CX3CR1 + subset was evaluated in Fstl1 +/ − ( n = 5) and WT littermates ( n = 5) at 48 h after MNC infusion. * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by a two-tailed unpaired t -test ( g – j ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Article Snippet: Single-cell suspensions were first incubated with anti-mouse FcR blocking reagent (BioLegend) and then labelled with the mixed fluorochrome-conjugated antibodies (BioLegend) PerCP/Cyanine5.5 anti-mouse CD45.2, PE/Cyanine 7 anti-mouse F4/80, FITC anti-mouse/human CD11b, APC/Cyanine 7 anti-mouse CX3CR1 and PE anti-mouse Ly6C, APC-conjugated anti-mouse CCR2, APC-conjugated anti-mouse CD45.1, PE-conjugated anti-mouse F4/80, PerCP/Cyanine5.5-conjugated anti-mouse Ly6C, Brilliant Violet 510-conjugated anti-mouse Ly-6G and the Zombie Aqua Fixable Viability Kit (BioLegend).

Techniques: Comparison, Expressing, Marker, Cell Counting, Flow Cytometry, Two Tailed Test

Journal: Signal Transduction and Targeted Therapy

Article Title: Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages

doi: 10.1038/s41392-025-02162-6

Figure Lengend Snippet: Inflammatory macrophages reprogram metabolism and improve the immunosuppressive capacity of MSCs. a Schematic illustration of the hepatic fibrosis model establishment and the MSC-based treatment strategy. b – d The degree of fibrosis was evaluated in the PBS-, MSC-, CsA+MSC-, and PF4136409 + MSC-treated groups at 4 weeks postinfusion ( n = 5). b Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Schematic of the in vitro coculture system for MSCs and BMDMs. f Volcano plot showing genes whose expression changed in MSCs cocultured with BMDMs compared with control MSCs, as determined by RNA-seq ( n = 4). g – j GSEA plots (left) and heatmaps (right) of the RNA-seq data of MSCs cocultured with BMDMs and control MSCs. Representative genes from each category are shown. FDR, false discovery rate; NES, normalized enrichment score. n = 4 mice per group. Statistical significance was determined by linear modelling and Bayesian statistics after correcting for multiple testing with the Benjamini–Hochberg procedure ( f ) or the Wald test with Benjamini–Hochberg’s multiple-comparison correction ( g – j ). k Gene expression was determined by qPCR in MSCs cocultured with increasing amounts of BMDMs ( n = 4). l Schematic of the in vitro coculture system for MSCs and BMDMs. m Gene expression was determined by qPCR in altered amounts of BMDMs cocultured with MSCs ( n = 4). n , o The percentages of the Ly6C − CX3CR1 + subset were determined via flow cytometry in altered amounts of BMDMs after coculture with MSCs ( n = 6). * p < 0.05, ** p < 0.01, *** p < 0.001, and n.s., not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( k , m , o ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Techniques: Staining, In Vitro, Expressing, Control, RNA Sequencing, Comparison, Gene Expression, Flow Cytometry

Journal: Signal Transduction and Targeted Therapy

Article Title: Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages

doi: 10.1038/s41392-025-02162-6

Figure Lengend Snippet: Administration of FSTL1 rescues the defective therapeutic effect of MSCs in Fstl1 +/ − mice. a Schematic illustration of hepatic fibrosis model establishment and the MSC-based early treatment strategy. b The fibrosis degree was evaluated in Fstl1 +/ − mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 4 weeks postinfusion. Liver sections were stained with Sirius red or Masson’s trichrome. Representative images of the staining are shown. Bars, 200 µm. c Liver fibrosis score analysis of Sirius red-stained liver sections. The fibrotic area is presented as a percentage. d The concentrations of hydroxyproline (HYP) in liver homogenates were determined. e Total liver RNA was extracted and the expression of Col1 and α-Sma was determined by qPCR. f – h Macrophage infiltration was evaluated in Fstl1 +/− mice treated with FSTL1 ( n = 5) or FSTL1 + PF4136409 ( n = 5) at 48 h post infusion. f The percentages of F4/80 + CD11b + cells among the total number of viable CD45 + cells and the number of CD11b + F4/80 + cells normalized to the liver weight were determined by flow cytometry. ( g ) The percentages of Ly6C − CX3CR1 + cells among the total number of viable CD45 + cells and the cell counts of the Ly6C − CX3CR1 + subset were compared. ( h ) F4/80 + macrophages were sorted from the livers of Fstl1 +/ − mice treated with FSTL1 or FSTL1 + PF4136409 at 24 h post infusion, and the mRNA levels of inflammatory markers ( Arg-1 , iNOS ) and Mmp9 were determined by qPCR. * p < 0.05, ** p < 0.01, and n.s. not significant. Statistical significance was determined by one-way ANOVA with Tukey multiple comparison test ( c , d , f , g ) or two-way ANOVA with Tukey multiple comparison test ( e , h ). Data are presented as the mean ± SEM and were pooled from at least three independent experiments

Techniques: Staining, Expressing, Flow Cytometry, Comparison

Intra-articular injection of ADSCs mitigated RA and restored the CX 3 CR1 + macrophage barrier in mice STA model. (A) RA clinical score when injecting ADSCs on day 0. (B) RA clinical score when injecting ADSCs on day 2. (C) Flow diagram of the in vivo injection experiment. (D) Swelling degree of mouse hind paws on day 8. (E) HE and SO/FG stanning results of histological sections of mouse knee and ankle joints on day 8. Scale bar, 200 μm. (F) The mRNA levels of pro-inflammatory factors in knee joint synovium on day 8. (G) The levels of pro-inflammatory and anti-inflammatory factors in peripheral blood on day 8. (H) Cryosection immunofluorescence stanning of CX 3 CR1 + lining macrophages in the knee joints of ADSCs and PBS injected mice using confocal laser scanning microscopy (CLSM) on day 8. Scale bar, 30 μm

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Figure Lengend Snippet: Intra-articular injection of ADSCs mitigated RA and restored the CX 3 CR1 + macrophage barrier in mice STA model. (A) RA clinical score when injecting ADSCs on day 0. (B) RA clinical score when injecting ADSCs on day 2. (C) Flow diagram of the in vivo injection experiment. (D) Swelling degree of mouse hind paws on day 8. (E) HE and SO/FG stanning results of histological sections of mouse knee and ankle joints on day 8. Scale bar, 200 μm. (F) The mRNA levels of pro-inflammatory factors in knee joint synovium on day 8. (G) The levels of pro-inflammatory and anti-inflammatory factors in peripheral blood on day 8. (H) Cryosection immunofluorescence stanning of CX 3 CR1 + lining macrophages in the knee joints of ADSCs and PBS injected mice using confocal laser scanning microscopy (CLSM) on day 8. Scale bar, 30 μm

Article Snippet: CAG-EGFP mice, Cx3cr1 cre Rosa26 ( R26 ) -tdTomato mice and Cx3cr1 cre R26-iDTR mice were all based on the C57BL/6J background and were purchased from Shanghai Model Organisms Center, Inc., Shanghai, China.

Techniques: Injection, In Vivo, Immunofluorescence, Confocal Laser Scanning Microscopy

ADSCs and CX 3 CR1 + lining macrophages co-localize both in vivo and in vitro. (A) Flow diagram of the strategy used to deplete CX 3 CR1 + lining macrophages and in vivo injection experiment. (B) RA clinical score after the depletion of CX 3 CR1 + lining macrophages. (C) Immunofluorescence stanning observation of the localization of ADSCs and CX 3 CR1 + lining macrophages in knee joints using CLSM on days 1–4 after ADSCs injection (on days 3–6). Scale bar, 50 μm. (D) Flow cytometry sorting of CX 3 CR1 + lining macrophages from animal tissues. (E) Co-culture of CX 3 CR1 + lining macrophages and ADSCs at a 1:1 ratio. Scale bar, 400 μm. (F) The spontaneously formed linear structure of CX 3 CR1 + lining macrophages in the co-culture system at a 1:1 ratio. Scale bar, 400 μm. (G-H) . Cell length and cell area of CX 3 CR1 + lining macrophages in different culture system

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Figure Lengend Snippet: ADSCs and CX 3 CR1 + lining macrophages co-localize both in vivo and in vitro. (A) Flow diagram of the strategy used to deplete CX 3 CR1 + lining macrophages and in vivo injection experiment. (B) RA clinical score after the depletion of CX 3 CR1 + lining macrophages. (C) Immunofluorescence stanning observation of the localization of ADSCs and CX 3 CR1 + lining macrophages in knee joints using CLSM on days 1–4 after ADSCs injection (on days 3–6). Scale bar, 50 μm. (D) Flow cytometry sorting of CX 3 CR1 + lining macrophages from animal tissues. (E) Co-culture of CX 3 CR1 + lining macrophages and ADSCs at a 1:1 ratio. Scale bar, 400 μm. (F) The spontaneously formed linear structure of CX 3 CR1 + lining macrophages in the co-culture system at a 1:1 ratio. Scale bar, 400 μm. (G-H) . Cell length and cell area of CX 3 CR1 + lining macrophages in different culture system

Techniques: In Vivo, In Vitro, Injection, Immunofluorescence, Flow Cytometry, Co-Culture Assay

Bulk transcriptome changes of ADSCs and CX 3 CR1 + lining macrophages after co-culture. (A) Cell viability difference between separately cultured and direct co-cultured cells after 96 h at 1:1 ratio. (B) GO analysis of upregulated genes in co-cultured ADSCs vs. separately cultured ADSCs (log2FC > 1, Padj < 0.05). (C) GO analysis of upregulated genes of co-cultured CX 3 CR1 + lining macrophages vs. individually cultured CX 3 CR1 + lining macrophages (log2FC > 1, Padj < 0.05). (D) CellChat chord diagram of cell-cell communication between ADSCs and CX 3 CR1 + lining macrophages based on the bulk RNA-seq data (Padj < 0.05)

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Figure Lengend Snippet: Bulk transcriptome changes of ADSCs and CX 3 CR1 + lining macrophages after co-culture. (A) Cell viability difference between separately cultured and direct co-cultured cells after 96 h at 1:1 ratio. (B) GO analysis of upregulated genes in co-cultured ADSCs vs. separately cultured ADSCs (log2FC > 1, Padj < 0.05). (C) GO analysis of upregulated genes of co-cultured CX 3 CR1 + lining macrophages vs. individually cultured CX 3 CR1 + lining macrophages (log2FC > 1, Padj < 0.05). (D) CellChat chord diagram of cell-cell communication between ADSCs and CX 3 CR1 + lining macrophages based on the bulk RNA-seq data (Padj < 0.05)

Techniques: Co-Culture Assay, Cell Culture, RNA Sequencing

ScRNA-seq analysis on the heterogeneity change of CX 3 CR1 + synovial lining macrophages in the barrier disruption and restoration process. (A) Annotated tSNE map of the subpopulations of synovial CD45 + CD11b + LY6G − cells. (B-C) tSNE map of CX 3 CR1 + lining macrophage subpopulations on STA days 1, 2, and 5. (D) Heatmap of differentially express genes in five subpopulations of CX 3 CR1 + lining macrophages (Padj < 0.05, top 10 most significantly differentially expressed). (E) The ratio of five cell subpopulations on STA days 1, 2, and 5. (F) GSEA analysis results showing hallmark changes of four cell subpopulations compared to Ccl24 high Fn1 low macrophages (Padj < 0.05). (G) Flow cytometry strategy for sorting synovial CD45 + CD11b + LY6G − cells. (H) The relative ratios of five cell subpopulations between the ADSCs and PBS injection groups. (I) Atf3/Cox5/Immt immunofluorescence stanning of knee joints of ADSCs and PBS injected mice on day 8

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Figure Lengend Snippet: ScRNA-seq analysis on the heterogeneity change of CX 3 CR1 + synovial lining macrophages in the barrier disruption and restoration process. (A) Annotated tSNE map of the subpopulations of synovial CD45 + CD11b + LY6G − cells. (B-C) tSNE map of CX 3 CR1 + lining macrophage subpopulations on STA days 1, 2, and 5. (D) Heatmap of differentially express genes in five subpopulations of CX 3 CR1 + lining macrophages (Padj < 0.05, top 10 most significantly differentially expressed). (E) The ratio of five cell subpopulations on STA days 1, 2, and 5. (F) GSEA analysis results showing hallmark changes of four cell subpopulations compared to Ccl24 high Fn1 low macrophages (Padj < 0.05). (G) Flow cytometry strategy for sorting synovial CD45 + CD11b + LY6G − cells. (H) The relative ratios of five cell subpopulations between the ADSCs and PBS injection groups. (I) Atf3/Cox5/Immt immunofluorescence stanning of knee joints of ADSCs and PBS injected mice on day 8

Techniques: Disruption, Flow Cytometry, Injection, Immunofluorescence

Mitochondrial transfer from ADSCs during the RA treatment process. A-E used CX 3 CR1 − synovial macrophages and F used CX 3 CR1 + synovial macrophages. (A) Transfer of mitochondria from WT-ADSCs (no fluorescence) stained with MitoTracker-Green to CX 3 CR1 − synovial macrophages in vitro. Scale bar, 20 μm. (B) . Transfer of mitochondria from EGFP-ADSCs (EGFP fluorescence) stained with MitoTracker-Red to CX 3 CR1 − synovial macrophages in vitro. Scale bar, 20 μm. (C) Inhibition of mitochondrial transfer from ADSCs by pretreatment with 10 µM nocodazole for 6 h. Scale bar, 40 μm. (D) Red fluorescence intensity of single CX 3 CR1 − lining macrophage in different groups. (E) Mitochondrial transfer from EGFP-Cox8-ADSCs to CX 3 CR1 − macrophages. Scale bar, 15 μm. (F) Mitochondrial transfer from EGFP-Cox8-ADSCs to CX 3 CR1 + lining macrophages. Scale bar, 30 & 10 μm, from left to right. (G) CLSM observation of mitochondrial transfer from EGFP-Cox8-ADSCs to synovial cells in vivo on STA day 4. Scale bar, 20 μm. (H) Isolated mitochondria of ADSCs stained with MitoTracker-Green. Scale bar, 100 μm. (I) RA clinical score changes when the TNTs of ADSCs were inhibited using nocodazole. (J) The role of the mitochondrial transplantation from ADSCs in RA treatment

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Figure Lengend Snippet: Mitochondrial transfer from ADSCs during the RA treatment process. A-E used CX 3 CR1 − synovial macrophages and F used CX 3 CR1 + synovial macrophages. (A) Transfer of mitochondria from WT-ADSCs (no fluorescence) stained with MitoTracker-Green to CX 3 CR1 − synovial macrophages in vitro. Scale bar, 20 μm. (B) . Transfer of mitochondria from EGFP-ADSCs (EGFP fluorescence) stained with MitoTracker-Red to CX 3 CR1 − synovial macrophages in vitro. Scale bar, 20 μm. (C) Inhibition of mitochondrial transfer from ADSCs by pretreatment with 10 µM nocodazole for 6 h. Scale bar, 40 μm. (D) Red fluorescence intensity of single CX 3 CR1 − lining macrophage in different groups. (E) Mitochondrial transfer from EGFP-Cox8-ADSCs to CX 3 CR1 − macrophages. Scale bar, 15 μm. (F) Mitochondrial transfer from EGFP-Cox8-ADSCs to CX 3 CR1 + lining macrophages. Scale bar, 30 & 10 μm, from left to right. (G) CLSM observation of mitochondrial transfer from EGFP-Cox8-ADSCs to synovial cells in vivo on STA day 4. Scale bar, 20 μm. (H) Isolated mitochondria of ADSCs stained with MitoTracker-Green. Scale bar, 100 μm. (I) RA clinical score changes when the TNTs of ADSCs were inhibited using nocodazole. (J) The role of the mitochondrial transplantation from ADSCs in RA treatment

Techniques: Fluorescence, Staining, In Vitro, Inhibition, In Vivo, Isolation, Transplantation Assay

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Techniques: Injection, In Vivo, Immunofluorescence, Confocal Laser Scanning Microscopy

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Techniques: In Vivo, In Vitro, Injection, Immunofluorescence, Flow Cytometry, Co-Culture Assay

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Techniques: Co-Culture Assay, Cell Culture, RNA Sequencing

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Techniques: Disruption, Flow Cytometry, Injection, Immunofluorescence

Journal: Stem Cell Research & Therapy

Article Title: Adipose-derived stem cells attenuate rheumatoid arthritis by restoring CX 3 CR1 + synovial lining macrophage barrier

doi: 10.1186/s13287-025-04144-5

Techniques: Fluorescence, Staining, In Vitro, Inhibition, In Vivo, Isolation, Transplantation Assay

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