Adiponectin inhibits TGF-β1-induced skin fibroblast proliferation and phenotype transformation via the p38 MAPK signaling pathway

The aim of this study was to investigate the effects of adiponectin (APN) on the proliferation and phenotypic transformation of human skin fibroblasts (HSFs) induced by TGF-beta 1. Primary fibroblast cultures were collected from prepuce surgery, and the cell viability and proliferative activity of HSFs were detected by Cell Counting Kit-8 and EdU assays. In addition, cell migration was detected by Transwell assay. The protein levels of related genes in HSF were detected by Western blotting. The results showed that the proliferation and migration abilities of HSF in the TGF-beta 1 group were significantly improved, and the relative protein expression levels of PCNA, alpha-SMA, and Collagen I in the TGF-beta 1 group were greatly increased. Furthermore, TGF-beta 1 stimulated the phosphorylation of p38 in HSF, while APN pretreatment significantly inhibited the TGF-beta 1-induced phosphorylation of p38. Additionally, blocking the p38 MAPK signaling pathway relieved the injury in the HSF induced by TGF-beta 1 and enhanced the therapeutic effect of APN in the TGF-beta 1-treated HSF. In conclusion, APN inhibits TGF-beta 1-induced HSF proliferation and myofibroblast phenotypic transformation by activating the p38 MAPK signaling pathway. APN is expected to become a potential target for preventing and treating skin fibrosis and pathological scars.