Overexpression of RACK1 inhibits collagen synthesis in keloid fibroblasts via inhibition of transforming growth factor-β1/Smad signaling pathway.

Abstract

Keloids are benign skin tumors characterized by collagen accumulation and hyperproliferation of fibroblasts. The receptor for activated C-kinase 1 (RACK1) was involved in liver fibrosis. However, the role of RACK1 in dermal fibrosis keloids is still unclear. Therefore, in this study, we investigated the effects of RACK1 on keloid fibroblasts (KFs) and transforming growth factor-β1 (TGF-β1)-induced collagen expression and explored the underlying mechanism. We found that RACK1 was decreased in KFs, overexpression of RACK1 significantly inhibited TGF-β1-induced KFs proliferation. RACK1 also obviously inhibited the expression of TGF-β1-induced TGF-β receptor I, II, type I collagen and α-smooth muscle actin (α-SMA) in human KFs. In addition, RACK1 suppressed the expression of TGF-β1-induced Smad2 and Smad3 phosphorylation in human KFs. Taken together, our study suggested that RACK1 inhibits collagen synthesis in KFs via inhibition the TGF-β1/Smad signaling pathway, and RACK1 is a potential target for treatment of the keloid disease.