长链非编码RNA-p21通过吸附微小RNA-18b促进糖尿病肾病进展。
LincRNA-p21 sponges miR-18b to promote the progression of diabetic nephropathy.
作者信息
Zhang Jingjing, Cao Xinling, Wang Shun, Aizimaiti Mikeryi, Xielifu Reyihan, Liu Jian
机构信息
Department of Nephropathy, The First Affiliated Hospital of Xinjiang Medical University Urumqi 830054, Xinjiang Uygur Autonomous Region, China.
出版信息
Am J Transl Res. 2018 May 15;10(5):1481-1489. eCollection 2018.
Little is known about the role of lincRNA-p21 in the development of diabetic nephropathy. The aim of the present study was to investigate the level of lincRNA-p21 in diabetic nephropathy, and explore its underlying mechanism. The current study revealed that down-regulation of lincRNA-p21 could alleviate pathological changes of diabetic nephropathy in mice. LincRNA-p21 expression was significantly up-regulated in MMCs under high glucose condition in . Besides, lincRNA-p21 promoted the proliferation of MMCs, which was reversed by miR-18b targeted with 3'-UTR. Moreover, miR-18b suppressed the expression of connective tissue growth factor (CTGF) by binding with the 3'-UTR. Furthermore, down-regulation of lincRNA-p21 expression alleviated extracellular matrix under high glucose, which could be reversed by miR-18b inhibitor significantly. In short, our study suggests lincRNA-p21 plays as an important role in progression of diabetic nephropathy in an animal model through interaction with miR-18b, providing a novel insight for the pathogenesis and an underlying therapeutic target for diabetic nephropathy.
关于长链非编码RNA-p21（lincRNA-p21）在糖尿病肾病发展中的作用，人们所知甚少。本研究的目的是调查糖尿病肾病中lincRNA-p21的水平，并探索其潜在机制。当前研究表明，lincRNA-p21的下调可减轻小鼠糖尿病肾病的病理变化。在高糖条件下，系膜细胞（MMCs）中lincRNA-p21的表达显著上调。此外，lincRNA-p21促进了MMCs的增殖，而这一作用被靶向3'-非翻译区（3'-UTR）的miR-18b所逆转。而且，miR-18b通过与3'-UTR结合抑制了结缔组织生长因子（CTGF）的表达。此外，lincRNA-p21表达的下调减轻了高糖环境下的细胞外基质，而这一作用可被miR-18b抑制剂显著逆转。简而言之，我们的研究表明lincRNA-p21在动物模型中通过与miR-18b相互作用，在糖尿病肾病进展中发挥重要作用，为糖尿病肾病的发病机制提供了新的见解以及潜在的治疗靶点。
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