...
首页> 外文期刊>Physiological Research >miR-29a is a potential protective factor for fibrogenesis in gluteal muscle contracture.
【24h】

miR-29a is a potential protective factor for fibrogenesis in gluteal muscle contracture.

机译:miR-29a是臀肌挛缩中纤维发生的潜在保护因素。

获取原文
           

摘要

Circulating miRNAs have been proposed as the effective diagnostic biomarkers for muscular fibrosis-associated diseases. However, circulating biomarkers for early diagnosis of contracture muscles are limited in gluteal muscle contracture (GMC) patients. Here we sought to explore the abnormally expressed miRNAs in plasma and contraction bands of GMC patients. The results showed miR-29a-3p expression in plasma and contraction bands tissue was significantly reduced in GMC patients compared with normal control. Cell viability and levels of proliferation-associated protein cyclin D1 and cyclindependent-kinase 2 (CDK2) were powerfully inhibited by miR-29a mimics and enhanced by miR-29a inhibitor compared with negative control. Furthermore, miR-29a mimics effectively impeded, while miR-29a inhibitor enhanced the expression of collagen I and collagen III, followed by the secretion of transforming growth factor β1 (TGF-β1), TGF-β3 and connective tissue growth factor (CTGF) in primary human contraction bands (CB) fibroblasts. The miR-29a-3p negatively regulated the expression of TGF-β1 through binding to the 3′ UTR region of SERPINH1 (encoding heat shock protein HSP47), but had no effect on Smad2 activity. The miR-29a-3p was inversely correlated with HSP47 in contraction bands tissue from GMC patients. Collectively, miR-29a was notably depressed and regulated cell viability and fibrosis by directly targeting HSP47 in GMC, which suggest that circulating miR-29a might be a potential biomarker for early diagnosis and provides a novel therapeutic target for GMC.
机译:循环的miRNA已被提议作为用于肌肉纤维化相关的疾病的有效的诊断生物标志物。然而,对于肌肉挛缩的早期诊断的生物标记物的循环中臀肌挛缩(GMC)的患者的限制。在这里,我们试图探讨在GMC患者血浆和收缩带的异常表达的miRNA。结果表明在血浆和收缩带组织的miR-29A-3P表达在GMC患者中降低显著与正常对照进行比较。细胞生存力和细胞周期蛋白D1和增殖相关蛋白的水平周期蛋白激酶2(CDK2)受miR-29A模拟物有力地抑制和增强的受miR-29A抑制剂与阴性对照进行比较。此外,的miR-29A模拟物有效地阻止,而的miR-29A抑制剂增强的胶原蛋白I和III型胶原的表达,随后转化生长因子β1(TGF-β1),TGF-β3和结缔组织生长因子的分泌(CTGF)在原代人收缩带(CB)的成纤维细胞。所述miR-29A-3P通过结合SERPINH1(编码热休克蛋白HSP47)的3'UTR区负调节TGF-β1的表达,但对Smad2的活性没有影响。与miR-29A-3P是在从患者GMC收缩带组织与HSP47呈负相关。总的来说,的miR-29A被压下显着,并通过在GMC,这表明循环的miR-29A可能是早期诊断潜在的生物标志物,并提供了新的治疗靶标。GMC的直接靶向HSP47调节细胞活力和纤维化。

著录项

获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号