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A – E Ventral confocal imaging (max projection) of representative 72 hpf hand2:EGFP;myl7DsRed larvae undergoing distinct treatments as indicated; anterior to the top; v ventricle, a atrium. A , B Representative larvae treated with DMSO vehicle only as control at 18 hpf overnight showing hand2:EGFP- expressing pericardial sac surrounding the heart at 72 hpf ( A , 20x) and cellular density ( B , 40x zoom, representative nuclei marked with dashed lines). C , D Ventral images of representative hand2:EGFP;myl7:DsRed larvae treated with the Wnt signaling inhibitor IWR-1 at 18 hpf overnight, showing expanded pericardial sac and edema with large, stretched cells surrounding the larval zebrafish heart at 72 hpf ( C 20x) and lower cellular density ( D 40x). E , F Ventral images of hand2:EGFP;myl7:DsRed larvae treated with BDM as myosin II inhibitor at 18 hpf overnight showing expanded pericardial sac with normal cell distribution at 72 hpf ( E 20x) and cellular density ( F 40x). G – J Quantifications of pericardial and cardiac features following the treatments. One-way ANOVA, n = 6 animals, three independent experiments. G Heart rate of vehicle-treated, Wnt-inhibited, and myosin II-inhibited (BDM) animals ( p = 0.6056 DMSO to IWR-1, p = 0.0001 DMSO to BDM). H Pericardial area (distribution per ventral view), showing increased pericardial area in IWR-1-treated animals ( p = 0.0631 DMSO to IWR-1, p = 0.317- DMSO to BDM). I Cell density (cells per square millimeter), showing decreased cell density in IWR-1-treated animals only ( p = 0.0001 DMSO to IWR-1, p = 0.01345 DMSO to BDM). J Cell size showing increases in IWR-1-treated embryos only ( p = 0.0001 DMSO to IWR-1, p = 0.9918 DMSO to BDM). K , L Increased tissue stiffness in the pericardium of rats treated with PBS (vehicle), Iso only, <t>sFRP1</t> only, or combined Isoproterenol (Iso) and SFRP1 ( n = 3 per condition). Neonatal rats (0-to-4-day old rats) were injected intraperitoneally with 0.05 mg/kg/day of human recombinant sFRP1 protein and Iso in an animal model of pediatric dilated cardiomyopathy. Atomic force microscopy (AFM) of dissected pericardia provided measures for Young’s modulus (kPa) as readout for tissue elasticity, with treated pericardia showing increased stiffness with combined Iso and sFRP1 only ( K ) as quantified per sample( L , unpaired two-tailed t -test, p = 0.9093 vehicle to Iso only, p = 0.6129 vehicle to sFRP1 only, p = 0.0140 vehicle to Iso + sFRP1). Each dot represents an individual sample. Representative images of control and = treated rats. Source data are provided as a Source Data file. Scale bar A , C , E 200 μm; B , D , F (40x) 50 μm. Species silhouettes were adapted from the PhyloPic database ( https://www.phylopic.org/ ).

Sfrp1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/sfrp1/product/R&D Systems
Average 93 stars, based on 27 article reviews

sfrp1 - by Bioz Stars, 2026-06

93/100 stars

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1) Product Images from "The pericardium forms as a distinct structure during heart formation"

Article Title: The pericardium forms as a distinct structure during heart formation

Journal: Nature Communications

doi: 10.1038/s41467-025-63599-5

Figure Legend Snippet: A – E Ventral confocal imaging (max projection) of representative 72 hpf hand2:EGFP;myl7DsRed larvae undergoing distinct treatments as indicated; anterior to the top; v ventricle, a atrium. A , B Representative larvae treated with DMSO vehicle only as control at 18 hpf overnight showing hand2:EGFP- expressing pericardial sac surrounding the heart at 72 hpf ( A , 20x) and cellular density ( B , 40x zoom, representative nuclei marked with dashed lines). C , D Ventral images of representative hand2:EGFP;myl7:DsRed larvae treated with the Wnt signaling inhibitor IWR-1 at 18 hpf overnight, showing expanded pericardial sac and edema with large, stretched cells surrounding the larval zebrafish heart at 72 hpf ( C 20x) and lower cellular density ( D 40x). E , F Ventral images of hand2:EGFP;myl7:DsRed larvae treated with BDM as myosin II inhibitor at 18 hpf overnight showing expanded pericardial sac with normal cell distribution at 72 hpf ( E 20x) and cellular density ( F 40x). G – J Quantifications of pericardial and cardiac features following the treatments. One-way ANOVA, n = 6 animals, three independent experiments. G Heart rate of vehicle-treated, Wnt-inhibited, and myosin II-inhibited (BDM) animals ( p = 0.6056 DMSO to IWR-1, p = 0.0001 DMSO to BDM). H Pericardial area (distribution per ventral view), showing increased pericardial area in IWR-1-treated animals ( p = 0.0631 DMSO to IWR-1, p = 0.317- DMSO to BDM). I Cell density (cells per square millimeter), showing decreased cell density in IWR-1-treated animals only ( p = 0.0001 DMSO to IWR-1, p = 0.01345 DMSO to BDM). J Cell size showing increases in IWR-1-treated embryos only ( p = 0.0001 DMSO to IWR-1, p = 0.9918 DMSO to BDM). K , L Increased tissue stiffness in the pericardium of rats treated with PBS (vehicle), Iso only, sFRP1 only, or combined Isoproterenol (Iso) and SFRP1 ( n = 3 per condition). Neonatal rats (0-to-4-day old rats) were injected intraperitoneally with 0.05 mg/kg/day of human recombinant sFRP1 protein and Iso in an animal model of pediatric dilated cardiomyopathy. Atomic force microscopy (AFM) of dissected pericardia provided measures for Young’s modulus (kPa) as readout for tissue elasticity, with treated pericardia showing increased stiffness with combined Iso and sFRP1 only ( K ) as quantified per sample( L , unpaired two-tailed t -test, p = 0.9093 vehicle to Iso only, p = 0.6129 vehicle to sFRP1 only, p = 0.0140 vehicle to Iso + sFRP1). Each dot represents an individual sample. Representative images of control and = treated rats. Source data are provided as a Source Data file. Scale bar A , C , E 200 μm; B , D , F (40x) 50 μm. Species silhouettes were adapted from the PhyloPic database ( https://www.phylopic.org/ ).

Techniques Used: Imaging, Control, Expressing, Injection, Recombinant, Animal Model, Microscopy, Two Tailed Test

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Journal: Nature Communications

Article Title: The pericardium forms as a distinct structure during heart formation

doi: 10.1038/s41467-025-63599-5

Figure Lengend Snippet: A – E Ventral confocal imaging (max projection) of representative 72 hpf hand2:EGFP;myl7DsRed larvae undergoing distinct treatments as indicated; anterior to the top; v ventricle, a atrium. A , B Representative larvae treated with DMSO vehicle only as control at 18 hpf overnight showing hand2:EGFP- expressing pericardial sac surrounding the heart at 72 hpf ( A , 20x) and cellular density ( B , 40x zoom, representative nuclei marked with dashed lines). C , D Ventral images of representative hand2:EGFP;myl7:DsRed larvae treated with the Wnt signaling inhibitor IWR-1 at 18 hpf overnight, showing expanded pericardial sac and edema with large, stretched cells surrounding the larval zebrafish heart at 72 hpf ( C 20x) and lower cellular density ( D 40x). E , F Ventral images of hand2:EGFP;myl7:DsRed larvae treated with BDM as myosin II inhibitor at 18 hpf overnight showing expanded pericardial sac with normal cell distribution at 72 hpf ( E 20x) and cellular density ( F 40x). G – J Quantifications of pericardial and cardiac features following the treatments. One-way ANOVA, n = 6 animals, three independent experiments. G Heart rate of vehicle-treated, Wnt-inhibited, and myosin II-inhibited (BDM) animals ( p = 0.6056 DMSO to IWR-1, p = 0.0001 DMSO to BDM). H Pericardial area (distribution per ventral view), showing increased pericardial area in IWR-1-treated animals ( p = 0.0631 DMSO to IWR-1, p = 0.317- DMSO to BDM). I Cell density (cells per square millimeter), showing decreased cell density in IWR-1-treated animals only ( p = 0.0001 DMSO to IWR-1, p = 0.01345 DMSO to BDM). J Cell size showing increases in IWR-1-treated embryos only ( p = 0.0001 DMSO to IWR-1, p = 0.9918 DMSO to BDM). K , L Increased tissue stiffness in the pericardium of rats treated with PBS (vehicle), Iso only, sFRP1 only, or combined Isoproterenol (Iso) and SFRP1 ( n = 3 per condition). Neonatal rats (0-to-4-day old rats) were injected intraperitoneally with 0.05 mg/kg/day of human recombinant sFRP1 protein and Iso in an animal model of pediatric dilated cardiomyopathy. Atomic force microscopy (AFM) of dissected pericardia provided measures for Young’s modulus (kPa) as readout for tissue elasticity, with treated pericardia showing increased stiffness with combined Iso and sFRP1 only ( K ) as quantified per sample( L , unpaired two-tailed t -test, p = 0.9093 vehicle to Iso only, p = 0.6129 vehicle to sFRP1 only, p = 0.0140 vehicle to Iso + sFRP1). Each dot represents an individual sample. Representative images of control and = treated rats. Source data are provided as a Source Data file. Scale bar A , C , E 200 μm; B , D , F (40x) 50 μm. Species silhouettes were adapted from the PhyloPic database ( https://www.phylopic.org/ ).

Article Snippet: The sFRP1 (Recombinant Human sFRP1 Protein, CF, R&D systems) solution was freshly prepared for each treatment by dissolving in phosphate-buffered saline (PBS) at room temperature.

Techniques: Imaging, Control, Expressing, Injection, Recombinant, Animal Model, Microscopy, Two Tailed Test

Sfrp1 regulates Vcam1 + fibro-adipogenic progenitor (FAP) adipogenic differentiation. (A) Dot plot demonstrating Wnt signaling pathways in Vcam1 + vs Vcam1 − FAPs. (B) Bar graph demonstrating Sfrp1 expression in Vcam1 + vs Vcam1 − FAPs. (C) Heatmap representing Pearson's correlation values of Sfrp1 and Vcam1 expression in FAPs. (D) Representative images of Oil Red O (ORO) staining of Vcam1 + FAPs treated with small interfering RNA ( siRNA ) against Sfrp1 and a control siRNA and quantification of ORO staining; data shown as mean ± standard error of the mean, ∗∗∗ P < .001. (E) Representative images of perilipin ( green ) and DAPI ( blue ) of Vcam1 + FAPs treated with siRNA against Sfrp1 and a control siRNA and quantification of perilipin staining; data shown as mean ± standard error of the mean, ∗ P < .05 (F) Representative images of peroxisome proliferator-activated receptor ( PPAR-γ ) ( green ) and DAPI ( blue ) of Vcam1 + FAPs treated with siRNA against Sfrp1 and a control siRNA and quantification of PPAR-γ staining; data shown as mean ± standard error of the mean, ∗∗∗ P < .001. n = 3 experimental replicates for D - F . OD , optical density.

Journal: JVS-Vascular Science

Article Title: Vascular adhesion molecule 1 + fibro-adipogenic progenitors mark fatty infiltration in chronic limb-threatening ischemia

doi: 10.1016/j.jvssci.2025.100295

Figure Lengend Snippet: Sfrp1 regulates Vcam1 + fibro-adipogenic progenitor (FAP) adipogenic differentiation. (A) Dot plot demonstrating Wnt signaling pathways in Vcam1 + vs Vcam1 − FAPs. (B) Bar graph demonstrating Sfrp1 expression in Vcam1 + vs Vcam1 − FAPs. (C) Heatmap representing Pearson's correlation values of Sfrp1 and Vcam1 expression in FAPs. (D) Representative images of Oil Red O (ORO) staining of Vcam1 + FAPs treated with small interfering RNA ( siRNA ) against Sfrp1 and a control siRNA and quantification of ORO staining; data shown as mean ± standard error of the mean, ∗∗∗ P < .001. (E) Representative images of perilipin ( green ) and DAPI ( blue ) of Vcam1 + FAPs treated with siRNA against Sfrp1 and a control siRNA and quantification of perilipin staining; data shown as mean ± standard error of the mean, ∗ P < .05 (F) Representative images of peroxisome proliferator-activated receptor ( PPAR-γ ) ( green ) and DAPI ( blue ) of Vcam1 + FAPs treated with siRNA against Sfrp1 and a control siRNA and quantification of PPAR-γ staining; data shown as mean ± standard error of the mean, ∗∗∗ P < .001. n = 3 experimental replicates for D - F . OD , optical density.

Article Snippet: FACS-sorted Vcam1 − FAPs were grown to 60% to 80% confluence followed by adipogenic differentiation and were treated with 500 ng/mL recombinant mouse Sfrp1 protein (R&D systems, 9019-SF) with or without sFRP-1 inhibitor, 2 μmol/L Way-316606 hydrochloride (Tocris, 4767), or vehicle control (DMSO).

Techniques: Protein-Protein interactions, Expressing, Staining, Small Interfering RNA, Control

Single cell RNA sequencing (RNA-seq) and single cell ATAC sequencing identifies Nr3c1 as a transcription factor (TF) that regulates fibro-adipogenic progenitor (FAP) adipogenesis. (A) Inferred TFs that regulate differential genes of Vcam1 + vs Vcam1 − FAPs. (B) Enhancers with regulation potential to Sfrp1 ( left ) and TF binding analysis to the enhancers. (C) Nr3c1 protein expression in Vcam1 + and Vcam1 − FAPs in adipogenic media for 3 days (n = technical replicates). (D) Representative images and quantification of Oil Red O (ORO) staining in Nr3c1-silenced Vcam1 + FAPs. Data shown as mean ± standard error of the mean, ∗∗ P < .01. (E and F) Representative images and quantification of perilipin ( green ), peroxisome proliferator-activated receptor gamma ( PPAR-γ ) ( green ), and DAPI ( blue ) staining in Nr3c1-silenced Vcam1 + FAPs. Data shown as mean ± standard error of the mean, ∗ P < .05, ∗∗∗ P < .001. n = 3 replicates for all experimental groups (C-F) . OD , optical density.

Journal: JVS-Vascular Science

Article Title: Vascular adhesion molecule 1 + fibro-adipogenic progenitors mark fatty infiltration in chronic limb-threatening ischemia

doi: 10.1016/j.jvssci.2025.100295

Figure Lengend Snippet: Single cell RNA sequencing (RNA-seq) and single cell ATAC sequencing identifies Nr3c1 as a transcription factor (TF) that regulates fibro-adipogenic progenitor (FAP) adipogenesis. (A) Inferred TFs that regulate differential genes of Vcam1 + vs Vcam1 − FAPs. (B) Enhancers with regulation potential to Sfrp1 ( left ) and TF binding analysis to the enhancers. (C) Nr3c1 protein expression in Vcam1 + and Vcam1 − FAPs in adipogenic media for 3 days (n = technical replicates). (D) Representative images and quantification of Oil Red O (ORO) staining in Nr3c1-silenced Vcam1 + FAPs. Data shown as mean ± standard error of the mean, ∗∗ P < .01. (E and F) Representative images and quantification of perilipin ( green ), peroxisome proliferator-activated receptor gamma ( PPAR-γ ) ( green ), and DAPI ( blue ) staining in Nr3c1-silenced Vcam1 + FAPs. Data shown as mean ± standard error of the mean, ∗ P < .05, ∗∗∗ P < .001. n = 3 replicates for all experimental groups (C-F) . OD , optical density.

Techniques: RNA Sequencing, Sequencing, Binding Assay, Expressing, Staining

Human chronic limb-threatening ischemia ( CLTI ) fibro-adipogenic progenitors ( FAPs ) display a myosteatosis transcriptional signature. (A) Uniform manifold approximation projection ( UMAP ) of FAPs in human PAD dataset, color represents subcluster. (B) UMAP of FAPs in human peripheral arterial disease ( PAD ) dataset, color represents location in limb. (C-E) Violin plot of Vcam1, Sfrp1, and Nr3c1 expression in distal/ischemic vs proximal/nonischemic FAPs. (F) Schematic summarizing study findings. Figures generated with Biorender.com .

Journal: JVS-Vascular Science

Article Title: Vascular adhesion molecule 1 + fibro-adipogenic progenitors mark fatty infiltration in chronic limb-threatening ischemia

doi: 10.1016/j.jvssci.2025.100295

Figure Lengend Snippet: Human chronic limb-threatening ischemia ( CLTI ) fibro-adipogenic progenitors ( FAPs ) display a myosteatosis transcriptional signature. (A) Uniform manifold approximation projection ( UMAP ) of FAPs in human PAD dataset, color represents subcluster. (B) UMAP of FAPs in human peripheral arterial disease ( PAD ) dataset, color represents location in limb. (C-E) Violin plot of Vcam1, Sfrp1, and Nr3c1 expression in distal/ischemic vs proximal/nonischemic FAPs. (F) Schematic summarizing study findings. Figures generated with Biorender.com .

Techniques: Expressing, Generated

Figure 4. The Wnt/β-catenin signaling in LepR+/CAR cells downregulated via CCRL2 in the presence of inﬂammation. (A) PCA of the RNA-Seq data of LepR+/CAR cells derived from WT and Ccrl2-KO mice after osteogenic induction and TNFα stimulation for 2 d. (B) Volcano plot showing differential gene expression in LepR+/CAR cells of WT and Ccrl2-KO mice. (C) Heatmap of top25 upregulated genes in LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (D) Heatmap of top25 downregulated genes in LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (E, F) GO-BP and KEGG enrichment analysis of the upregulated differentially expressed genes of LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (G, H) Western blot analysis (n = 3) of CCRL2, SFRP1, Wnt/β-catenin signaling-related proteins, and OSX expression levels with or without TNFα stimulation in LepR+/CAR cells of WT and Ccrl2-KO mice. (I) Immunoﬂuorescence staining of LepR and SFRP1 in the extraction sockets of Ccrl2-KO and WT mice 3 d postextraction (scale bar: left, 120 μm; right, 15 μm). (J) Immunoﬂuorescence staining of LepR and active β-catenin in the extraction sockets of Ccrl2-KO and WT mice 3 d postextraction (scale bar: left, 120 μm; right, 15 μm). (K) Immunoﬂuorescence staining of SFRP1 in human healthy gingival tissues, periodontitis gingival tissues, and periodontitis extraction socket tissues (scale bar: left, 80 μm; right, 15 μm). (L) Percentage of SFRP1+LepR+/LepR+ cells in the extraction sockets of Ccrl2-KO and WT mice (n = 6). (M) Percentage of active β-catenin+LepR+/LepR+ cells in the extraction sockets of Ccrl2-KO and WT mice (n = 6). (N) Percentage of SFRP1+/DAPI+ cells in healthy gingival tissues, periodontitis gingival tissues, and periodontitis extraction socket tissues (n = 6).

Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

Article Title: LepR+ stromal cells respond to periodontitis and attenuate alveolar bone repair via CCRL2 mediated Wnt inhibition.

doi: 10.1093/jbmr/zjae036

Figure Lengend Snippet: Figure 4. The Wnt/β-catenin signaling in LepR+/CAR cells downregulated via CCRL2 in the presence of inﬂammation. (A) PCA of the RNA-Seq data of LepR+/CAR cells derived from WT and Ccrl2-KO mice after osteogenic induction and TNFα stimulation for 2 d. (B) Volcano plot showing differential gene expression in LepR+/CAR cells of WT and Ccrl2-KO mice. (C) Heatmap of top25 upregulated genes in LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (D) Heatmap of top25 downregulated genes in LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (E, F) GO-BP and KEGG enrichment analysis of the upregulated differentially expressed genes of LepR+/CAR cells of Ccrl2-KO mice compared with WT mice. (G, H) Western blot analysis (n = 3) of CCRL2, SFRP1, Wnt/β-catenin signaling-related proteins, and OSX expression levels with or without TNFα stimulation in LepR+/CAR cells of WT and Ccrl2-KO mice. (I) Immunoﬂuorescence staining of LepR and SFRP1 in the extraction sockets of Ccrl2-KO and WT mice 3 d postextraction (scale bar: left, 120 μm; right, 15 μm). (J) Immunoﬂuorescence staining of LepR and active β-catenin in the extraction sockets of Ccrl2-KO and WT mice 3 d postextraction (scale bar: left, 120 μm; right, 15 μm). (K) Immunoﬂuorescence staining of SFRP1 in human healthy gingival tissues, periodontitis gingival tissues, and periodontitis extraction socket tissues (scale bar: left, 80 μm; right, 15 μm). (L) Percentage of SFRP1+LepR+/LepR+ cells in the extraction sockets of Ccrl2-KO and WT mice (n = 6). (M) Percentage of active β-catenin+LepR+/LepR+ cells in the extraction sockets of Ccrl2-KO and WT mice (n = 6). (N) Percentage of SFRP1+/DAPI+ cells in healthy gingival tissues, periodontitis gingival tissues, and periodontitis extraction socket tissues (n = 6).

Article Snippet: In the recombinant SFRP1 (rSFRP1)-treated group, 1 μg/mL recombinant mouse SFRP1 protein (R&D Systems, USA) was added to the osteogenic induction medium.

Techniques: RNA Sequencing, Derivative Assay, Gene Expression, Western Blot, Expressing, Staining, Extraction

Figure 5. The CCRL2 in LepR+/CAR cells inhibits osteogenesis by binding to SFRP1 to suppress Wnt/β-catenin signaling under inﬂammation. (A) Coimmunoprecipitation analysis of the interaction between CCRL2 and SFRP1 in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation. (B) GST pull-down assay conﬁrmed the binding of recombinant GST-SFRP1 and CCRL2 derived from the lysates of LepR+/CAR cells under TNFα induced inﬂammation. (C) CCRL2 and SFRP1were coimmunoprecipitated using Wnt3a antibody in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation. (D, E) Western blot analysis (n = 3) of the changes in CCRL2, Wnt/β-catenin signaling-related proteins, and OSX expression levels in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation in the presence of rSFRP1. (F) Statistical analysis (n = 3) of the inhibition rates of active β-catenin, p-GSK3β-Ser9, and OSX protein expression in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (G, H) ALP staining and analysis (n = 3) of ALP activity after osteogenic induction for 7 d in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (I, J) ARS staining and OD value test (n = 3) after 21 d of osteogenic induction in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (K, L) Western blot analysis (n = 3) of the changes in Wnt/β-catenin signaling-related proteins and OSX expression levels in LepR+/CAR cells of Ccrl2-KO and WT mice with or without Wnt3a stimulation in the presence of TNFα. (M) Statistical analysis (n = 3) of the activation rates of active β-catenin, p-GSK3β-Ser9, and OSX protein expression in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of Wnt3a.

Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

Article Title: LepR+ stromal cells respond to periodontitis and attenuate alveolar bone repair via CCRL2 mediated Wnt inhibition.

doi: 10.1093/jbmr/zjae036

Figure Lengend Snippet: Figure 5. The CCRL2 in LepR+/CAR cells inhibits osteogenesis by binding to SFRP1 to suppress Wnt/β-catenin signaling under inﬂammation. (A) Coimmunoprecipitation analysis of the interaction between CCRL2 and SFRP1 in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation. (B) GST pull-down assay conﬁrmed the binding of recombinant GST-SFRP1 and CCRL2 derived from the lysates of LepR+/CAR cells under TNFα induced inﬂammation. (C) CCRL2 and SFRP1were coimmunoprecipitated using Wnt3a antibody in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation. (D, E) Western blot analysis (n = 3) of the changes in CCRL2, Wnt/β-catenin signaling-related proteins, and OSX expression levels in LepR+/CAR cells of Ccrl2-KO and WT mice with or without TNFα stimulation in the presence of rSFRP1. (F) Statistical analysis (n = 3) of the inhibition rates of active β-catenin, p-GSK3β-Ser9, and OSX protein expression in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (G, H) ALP staining and analysis (n = 3) of ALP activity after osteogenic induction for 7 d in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (I, J) ARS staining and OD value test (n = 3) after 21 d of osteogenic induction in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of rSFRP1. (K, L) Western blot analysis (n = 3) of the changes in Wnt/β-catenin signaling-related proteins and OSX expression levels in LepR+/CAR cells of Ccrl2-KO and WT mice with or without Wnt3a stimulation in the presence of TNFα. (M) Statistical analysis (n = 3) of the activation rates of active β-catenin, p-GSK3β-Ser9, and OSX protein expression in LepR+/CAR cells of Ccrl2-KO and WT mice with TNFα stimulation in the presence of Wnt3a.

Article Snippet: In the recombinant SFRP1 (rSFRP1)-treated group, 1 μg/mL recombinant mouse SFRP1 protein (R&D Systems, USA) was added to the osteogenic induction medium.

Techniques: Binding Assay, Pull Down Assay, Recombinant, Derivative Assay, Western Blot, Expressing, Inhibition, Staining, Activity Assay, Activation Assay

Figure 6. Inhibiting SFRP1 signaling in LepR+/CAR cells promotes alveolar bone healing in extraction sockets with periodontitis. (A) Schematic diagram of the experimental procedure to inject the SFRP1 inhibitor WAY-316606 into the extraction sockets of LepR-Cre; tdTomato mice. (B) Micro-CT images of extraction sockets in the vehicle and WAY-316606 group 14 d postextraction; sagittal view (upper) and coronal view (lower). Dashed lines indicate extraction sockets and the arrows indicate extraction sockets with periodontitis (scale bar: 200 μm). (C) Micro-CT analysis (n = 6) of bone healing in the vehicle and WAY-316606 groups. (D) Immunoﬂuorescence staining of CCRL2 and OSX in the extraction sockets of the vehicle and WAY-316606 groups 3 d postextraction. LepR-td represents LepR+/CAR cells (scale bar: left, 120 μm; right, 15 μm). (E) Immunoﬂuorescence staining of active β-catenin in the extraction sockets of the vehicle and WAY-316606 groups 3 d postextraction. LepR-td represents LepR+/CAR cells (scale bar: left, 120 μm; right, 15 μm). (F) Percentage of OSX+ LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (G) Percentage of CCRL2+ LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (H) Percentage of active β-catenin+LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (I) Schematic diagram illustrating the mechanism by which CCRL2 inhibits the osteogenic differentiation of LepR+/CAR cells during tooth extraction socket healing with periodontitis. (n = 6 for each group.)

Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

Article Title: LepR+ stromal cells respond to periodontitis and attenuate alveolar bone repair via CCRL2 mediated Wnt inhibition.

doi: 10.1093/jbmr/zjae036

Figure Lengend Snippet: Figure 6. Inhibiting SFRP1 signaling in LepR+/CAR cells promotes alveolar bone healing in extraction sockets with periodontitis. (A) Schematic diagram of the experimental procedure to inject the SFRP1 inhibitor WAY-316606 into the extraction sockets of LepR-Cre; tdTomato mice. (B) Micro-CT images of extraction sockets in the vehicle and WAY-316606 group 14 d postextraction; sagittal view (upper) and coronal view (lower). Dashed lines indicate extraction sockets and the arrows indicate extraction sockets with periodontitis (scale bar: 200 μm). (C) Micro-CT analysis (n = 6) of bone healing in the vehicle and WAY-316606 groups. (D) Immunoﬂuorescence staining of CCRL2 and OSX in the extraction sockets of the vehicle and WAY-316606 groups 3 d postextraction. LepR-td represents LepR+/CAR cells (scale bar: left, 120 μm; right, 15 μm). (E) Immunoﬂuorescence staining of active β-catenin in the extraction sockets of the vehicle and WAY-316606 groups 3 d postextraction. LepR-td represents LepR+/CAR cells (scale bar: left, 120 μm; right, 15 μm). (F) Percentage of OSX+ LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (G) Percentage of CCRL2+ LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (H) Percentage of active β-catenin+LepR-td+/LepR-td+ cells in the vehicle and WAY-316606 groups. (I) Schematic diagram illustrating the mechanism by which CCRL2 inhibits the osteogenic differentiation of LepR+/CAR cells during tooth extraction socket healing with periodontitis. (n = 6 for each group.)

Article Snippet: In the recombinant SFRP1 (rSFRP1)-treated group, 1 μg/mL recombinant mouse SFRP1 protein (R&D Systems, USA) was added to the osteogenic induction medium.

Techniques: Extraction, Micro-CT, Staining

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1) Product Images from "The pericardium forms as a distinct structure during heart formation"

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