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

被引：2
作者：
Zhou, Ping [1 ]
Shi, Lina [2 ]
Li, Qing [3 ]
Lu, Di [1 ]
机构：
[1] First Hosp Zibo City, Dept Dermatol, Zibo 255220, Shandong, Peoples R China
[2] First Hosp Zibo City, Dept Hematopathy, Zibo 255220, Shandong, Peoples R China
[3] First Hosp Zibo City, Cent Lab, Zibo 255220, Shandong, Peoples R China
来源：
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2015年 / 8卷 / 09期
关键词：
RACK1; keloid fibroblasts (KFs); collagen synthesis; TGF-beta 1/Smad signaling pathway; TGF-BETA; ALPHA-SMA; EXPRESSION; PROTEIN; PROLIFERATION; RECEPTOR;
D O I：
暂无
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
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-beta 1 (TGF-beta 1)-induced collagen expression and explored the underlying mechanism. We found that RACK1 was decreased in KFs, overexpression of RACK1 significantly inhibited TGF-beta 1-induced KFs proliferation. RACK1 also obviously inhibited the expression of TGF-beta 1-induced TGF-beta receptor I, II, type I collagen and a-smooth muscle actin (alpha-SMA) in human KFs. In addition, RACK1 suppressed the expression of TGF-beta 1-induced Smad2 and Smad3 phosphorylation in human KFs. Taken together, our study suggested that RACK1 inhibits collagen synthesis in KFs via inhibition the TGF-beta 1/Smad signaling pathway, and RACK1 is a potential target for treatment of the keloid disease.
引用
收藏
页码：15262 / 15268
页数：7
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