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

IF 0.2 Q4 MEDICINE, RESEARCH & EXPERIMENTAL

International journal of clinical and experimental medicine Pub Date : 2015-09-15 eCollection Date: 2015-01-01

Ping Zhou, Lina Shi, Qing Li, Di Lu

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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.

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通过抑制转化生长因子-β1/Smad 信号通路，过表达 RACK1 可抑制瘢痕疙瘩成纤维细胞中胶原蛋白的合成。

瘢痕疙瘩是一种良性皮肤肿瘤，其特点是胶原蛋白堆积和成纤维细胞过度增殖。活化 C 激酶 1 受体（RACK1）参与了肝纤维化。然而，RACK1 在皮肤纤维化瘢痕疙瘩中的作用仍不清楚。因此，在本研究中，我们研究了 RACK1 对瘢痕疙瘩成纤维细胞（KFs）和转化生长因子-β1（TGF-β1）诱导的胶原表达的影响，并探讨了其潜在机制。我们发现，RACK1在KFs中含量降低，过表达RACK1能显著抑制TGF-β1诱导的KFs增殖。RACK1 还能明显抑制 TGF-β1 诱导的 TGF-β 受体 I、II、I 型胶原和α-平滑肌肌动蛋白（α-SMA）在人 KFs 中的表达。此外，RACK1 还能抑制 TGF-β1 诱导的 Smad2 和 Smad3 在人 KFs 中的磷酸化表达。综上所述，我们的研究表明，RACK1通过抑制TGF-β1/Smad信号通路抑制KFs中胶原蛋白的合成，RACK1是治疗瘢痕疙瘩病的潜在靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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International journal of clinical and experimental medicine MEDICINE, RESEARCH & EXPERIMENTAL-

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