Journal: Journal of Translational Medicine
Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism
doi: 10.1186/s12967-025-06804-9
Figure Lengend Snippet: CCN5 regulates activation of TGF-β/Smad and Wnt/β-catenin signaling pathways. A , B Luciferase reporter assays in primary HESCs transfected with the indicated plasmids and treated with the vehicle, TGF-β or prifenidone. FLuc/RLuc activity was determined as mean ± SEM. Statistical analysis was performed using one-way ANOVA. * p < 0.05, ** p < 0.01. C, D. The mRNA expression of downstream target genes of TGF-β/Smad and Wnt/β-catenin signaling pathways in CCN5-overexpression HESCs ( C ) or CCN5-knockdown HESCs ( D ) treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. * p < 0.05, ** p < 0.01. E, F. The protein expression of p-Smad3, Smad3, p-β-catenin and β-catenin in CCN5-overexpression HESCs ( E ) or CCN5-knockdown HESCs ( F ) treated with TGF-β or without TGF-β. G. The protein expression of β-catenin in cytoplasmic and nuclear part of CCN5-overexpression HESCs or CCN5-knockdown HESCs was measured by western blotting
Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).
Techniques: Activation Assay, Protein-Protein interactions, Luciferase, Transfection, Activity Assay, Expressing, Over Expression, Knockdown, Western Blot