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recombinant mouse sfrp1 protein (R&D Systems)

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R&D Systems recombinant mouse sfrp1 protein

<t>Sfrp1</t> 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.

Recombinant Mouse Sfrp1 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+sfrp+1+protein/Recombinant+Mouse+sFRP-1+Protein/pmc12446680-66-21-25
Average 93 stars, based on 7 article reviews

recombinant mouse sfrp1 protein - by Bioz Stars, 2026-09

93/100 stars

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1) Product Images from "Vascular adhesion molecule 1 + fibro-adipogenic progenitors mark fatty infiltration in chronic limb-threatening ischemia"

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

Journal: JVS-Vascular Science

doi: 10.1016/j.jvssci.2025.100295

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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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 Used: 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 .

Figure Legend 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 Used: Expressing, Generated

Organ Culture:

Article Title: Quantitative modeling of regular retinal microglia distribution
Article Snippet: We added Ib4 lectin (1/1000, Invitrogen I21411) to stain both resting and activated microglia. .. Reagents used in the organ culture experiments are: Phosphatidylinositol-specific Phospholipase C from Bacillus cereus (PI-PLC, 0.5 U/ml, Sigma-Aldrich P5542), Recombinant Mouse sFRP-1 Protein (1 μg/ml, R&D Systems, MN9019-SF-025), Plexin-D1 Fc fragment (30 μg/ml), Alexa Fluor 647-ATP (5 μM, Invitrogen A22362), and Clopidogrel (25 μM, TOCRIS 249010). .. We quantified the ATP uptake and diffusion using Alexa Fluor 647-ATP (Invitrogen A22362).

Article Title: Quantitative modeling of regular retinal microglia distribution
Article Snippet: We added Ib4 lectin (1/1000, Invitrogen I21411) to stain microglia. .. Reagents used in the organ culture experiments are: Phosphatidylinositol-specific Phospholipase C from Bacillus cereus (PI-PLC, 0.5 U/ml, Sigma-Aldrich P5542), Recombinant Mouse sFRP-1 Protein (1 μg/ml, R&D Systems, MN9019-SF-025), Plexin-D1 Fc fragment (30 μg/ml), Alexa Fluor 647-ATP (5 μM, Invitrogen A22362), and Clopidogrel (25 μM, TOCRIS 249010). ..

Recombinant:

Article Title: Vcam1+ Fibro-adipogenic Progenitors Mark Fatty Infiltration in Chronic Limb Threatening Ischemia
Article Snippet: FACS-sorted Vcam1+ FAP cells were grown to 60-80% confluence and transfected with 40 nM Accell mouse Sfrp1 siRNA SMARTPool (Dharmacon, E-048941-00-0005), 50 nM ON-TARGET plus mouse Nr3c1 siRNA SMARTPool (Dharmacon, L-045970-01-0005) and 50 nM ON-TARGET plus Non-targeting Control siRNAs (Dharmacon, D-001810-04-05) diluted in Opti-MEMTM I Reduced Serum Medium (ThermoFisher Scientific, 11058021) and transfected with LipofectamineTM RNAiMAX Transfection Reagent (Invitrogen, 13778030) per the manufacture’s recommendation for 48 to 72 hours. .. FACS-sorted Vcam1-FAPs were grown to 60-80% confluence followed by adipogenic differentiation and were treated with 500 ng/mL recombinant mouse sFRP-1 protein (R&D systems, 9019-SF) with or without sFRP-1 inhibitor, 2 uM Way-316606 hydrochloride (Tocris, 4767) or vehicle control (DMSO). ..

FACS:

Control:

Image Search Results

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

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

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

Fig. 7. Effects of recombinant Wnt1 on critical-size bone defect healing. (A) Experimental design. (B) Representative 3D reconstructions from μCT datasets. The entire area between the two inner pin holes in shown. Red indicates less mineralized bone, whereas yellow and blue indicate higher mineralized bone. (C) Bone volume in the defect area. (D) Polar moment of inertia of the bone in the defect area as analyzed by μCT evaluation. (E) Trabecular thickness, (F) trabecular separation, and (G) trabecular number of the newly formed bone in the defect area. (H) Active YAP1 and BMP2 immunostaining in the defect area. Scale bar = 100 μm. n = 7 per group. Mann-Whitney U test. sFRP1, secreted frizzled-related protein 1.

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

Article Title: Wnt1 Boosts Fracture Healing by Enhancing Bone Formation in the Fracture Callus.

doi: 10.1002/jbmr.4797

Figure Lengend Snippet: Fig. 7. Effects of recombinant Wnt1 on critical-size bone defect healing. (A) Experimental design. (B) Representative 3D reconstructions from μCT datasets. The entire area between the two inner pin holes in shown. Red indicates less mineralized bone, whereas yellow and blue indicate higher mineralized bone. (C) Bone volume in the defect area. (D) Polar moment of inertia of the bone in the defect area as analyzed by μCT evaluation. (E) Trabecular thickness, (F) trabecular separation, and (G) trabecular number of the newly formed bone in the defect area. (H) Active YAP1 and BMP2 immunostaining in the defect area. Scale bar = 100 μm. n = 7 per group. Mann-Whitney U test. sFRP1, secreted frizzled-related protein 1.

Article Snippet: The critical-size model has been described. (31) Five micrograms (5 μg) of recombinant sFRP1 protein alone (R&D Systems; 9019-SF-025) was used for the control group.

Techniques: Recombinant, Immunostaining, MANN-WHITNEY

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recombinant mouse sfrp1 protein (R&D Systems)

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1) Product Images from "Vascular adhesion molecule 1 + fibro-adipogenic progenitors mark fatty infiltration in chronic limb-threatening ischemia"

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