Mouse TRAIL/TNFSF10 Antibody

TRAIL/TNFSF10 in Mouse Thymus. TRAIL/TNFSF10 was detected in perfusion fixed frozen sections of mouse thymus using Goat Anti-Mouse TRAIL/TNFSF10 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1121) at 1.5 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Goat HRP-DAB Cell & Tissue Staining Kit (brown; CTS008) and counterstained with hematoxylin (blue). View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections.

Detection of Mouse TRAIL/TNFSF10 by Immunohistochemistry OSCAR–collagen binding co-stimulates IL-1 beta -induced apoptotic signaling in articular chondrocytes.a Caspase activity in mouse articular chondrocytes treated with IL-1 beta (5 ng mL−1) and collagenase (Coll, 50 U mL−1). b, c qRT-PCR analysis (b) and western blotting (c) in mouse articular chondrocytes. Chondrocytes were either untreated or transfected with control siRNA (C-siRNA) (100 nM) or siRNAs specific for mouse Oscar and exposed to IL-1 beta (5 ng mL−1) and collagenase (50 U mL−1) for 48 h. d Articular chondrocyte viability was quantified by MTT assay. Error bars represent mean ± S.E.M. of n = 5 wells. e Caspase-8 and caspase-3 activity was measured using the respective assay kits. f, g qRT-PCR analysis (f) and western blotting (g) in mouse articular chondrocytes. Chondrocytes were treated with hIgG or hOSCAR-Fc (10 μg ml−1) with collagenase and exposed to IL-1 beta for 48 h. h Apoptotic articular chondrocytes were detected and quantified by TUNEL assay. Scale bar = 100 μm. i, j qRT-PCR analysis (i) and western blotting (j) in mouse articular chondrocytes treated with 10 μΜ OSCAR-binding triple-helical peptide before IL-1 beta treatment. Articular chondrocytes were treated with hOSCAR-Fc for 48 h. Error bars shown in a, b, e, f, h and i are mean ± S.E.M. for n = 4 independent experiments. One-way ANOVA was performed followed by Dunnett’s Multiple Comparison’s test (a, i) and Tukey’s Multiple Comparison’s test (b, d, e, f, h), with p values indicated in figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32859940), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse TRAIL/TNFSF10 by Immunohistochemistry OSCAR regulates OA pathogenesis via TRAIL-induced articular chondrocyte apoptosis.a Selection of putative Oscar targets involved in OA pathogenesis. Venn diagram indicating the number of genes attenuated in articular cartilage Oscar−/− mice after DMM surgery (left). Hypergeometric p value measuring the significance of enrichment is depicted. Gene-wise scaled gene expression patterns of 1270 common genes in each sample are shown (right). b Functional annotations significantly enriched for 1270 common genes. Hypergeometric tests were performed using the hallmark gene annotation in MsigDB, yielding enrichment scores, defined as −log10 (FDR). c Simplified apoptotic signaling pathway altered by Oscar deficiency. Each gene is colored with the DIF score, defined as the extent to which gene expression is altered by Oscar deficiency. A negative DIF indicates transcriptional suppression in Oscar−/− mice. The network was visualized by Cytoscape v3.7 software. d, e qRT-PCR (d) and IHC (e) analyses of TRAIL in OA articular cartilage from DMM surgery mice compared to sham-operated mice. Scale bar = 50 μm. f, g mRNA levels (f) and immunostaining (g) for OPG in articular cartilage tissue from sham surgery or DMM surgery mice. Scale bar = 50 μm. h, i Apoptotic articular chondrocytes were detected and quantified by TUNEL assay. Scale bar = 25 μm. Error bars represent mean ± S.E.M. of n = 10 mice (d–g, i). Two-way ANOVA was performed followed by Sidak’s Multiple Comparison’s test, with p values indicated in figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32859940), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse TRAIL/TNFSF10 by Immunohistochemistry OSCAR regulates OA pathogenesis via TRAIL-induced articular chondrocyte apoptosis.a Selection of putative Oscar targets involved in OA pathogenesis. Venn diagram indicating the number of genes attenuated in articular cartilage Oscar−/− mice after DMM surgery (left). Hypergeometric p value measuring the significance of enrichment is depicted. Gene-wise scaled gene expression patterns of 1270 common genes in each sample are shown (right). b Functional annotations significantly enriched for 1270 common genes. Hypergeometric tests were performed using the hallmark gene annotation in MsigDB, yielding enrichment scores, defined as −log10 (FDR). c Simplified apoptotic signaling pathway altered by Oscar deficiency. Each gene is colored with the DIF score, defined as the extent to which gene expression is altered by Oscar deficiency. A negative DIF indicates transcriptional suppression in Oscar−/− mice. The network was visualized by Cytoscape v3.7 software. d, e qRT-PCR (d) and IHC (e) analyses of TRAIL in OA articular cartilage from DMM surgery mice compared to sham-operated mice. Scale bar = 50 μm. f, g mRNA levels (f) and immunostaining (g) for OPG in articular cartilage tissue from sham surgery or DMM surgery mice. Scale bar = 50 μm. h, i Apoptotic articular chondrocytes were detected and quantified by TUNEL assay. Scale bar = 25 μm. Error bars represent mean ± S.E.M. of n = 10 mice (d–g, i). Two-way ANOVA was performed followed by Sidak’s Multiple Comparison’s test, with p values indicated in figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32859940), licensed under a CC-BY license. Not internally tested by R&D Systems.