Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF-β1-Induced Propagation and Migration in Keloid Fibroblasts.

4区医学 Q3 Medicine Disease Markers Pub Date : 2023-04-12 eCollection Date: 2023-01-01 DOI:10.1155/2023/9638322

Lin He, Chan Zhu, Huicong Dou, Xueyuan Yu, Jing Jia, Maoguo Shu

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引用次数: 1

Abstract

Purpose: Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.

Methods: KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-β1 stimulation group, KFs were processed with human recombinant TGF-β1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.

Results: CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-β1-induced propagation and migration in KFs. Col I, α-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-β1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-β receptors TRI and TRII in TGF-β1-induced KFs. Furthermore, CTRP3 prevented TGF-β1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.

Conclusion: CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.

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瘢痕疙瘩核心因子 CTRP3 的过表达能显著控制 TGF-β1 诱导的瘢痕疙瘩成纤维细胞的繁殖和迁移。

目的：瘢痕疙瘩是一种以过度瘢痕增生为特征的良性纤维增生性肿瘤。C1q/TNF相关蛋白3（CTRP3）已被证实具有抗纤维化作用。在此，我们探讨了 CTRP3 在瘢痕疙瘩中的作用。在本研究中，我们探讨了CTRP3对瘢痕疙瘩成纤维细胞（KFs）的影响，并研究了其潜在的分子机制：方法：收集 10 名瘢痕疙瘩患者的 KF 组织标本和邻近的正常成纤维细胞（NF）组织。在 TGF-β1 刺激组，用人重组 TGF-β1 处理 KF。进行 pcDNA3.1-CTRP3 或 pcDNA3.1 细胞转染。si-CTRP3）或阴性对照 siRNA（si-scramble）转染 KFs：结果：CTRP3在瘢痕疙瘩组织和KFs中下调。结果：CTRP3在瘢痕疙瘩组织和KFs中下调，过表达CTRP3可明显控制TGF-β1诱导的KFs繁殖和迁移。Col I、α-SMA和纤连蛋白的mRNA和蛋白水平在TGF-β1刺激下升高，而CTRP3过表达则抑制了它们的升高。相反，CTRP3 基因敲除则表现出相反的效果。此外，在 TGF-β1 诱导的 KFs 中，CTRP3 可抑制 TGF-β 受体 TRI 和 TRII。此外，CTRP3还阻止了TGF-β1刺激的smad2和smad3的核转位，并抑制了KFs中p-smad2和p-smad3的表达水平：结论：CTRP3通过调节TGF-β1/Smad信号通路，抑制KFs的增殖、迁移和ECM积累，从而发挥抗纤维化作用。

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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来源期刊

Disease Markers 医学-病理学

自引率

0.00%

发文量

792

审稿时长

6-12 weeks

期刊介绍： Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.