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长链非编码 RNA MALAT1 通过 miR-378a-3p 上调 PDE6G 促进糖尿病视网膜病变。

lncRNA MALAT1 promotes diabetic retinopathy by upregulating PDE6G via miR-378a-3p.

机构信息

Department of Ophthalmology, Wuhan Third Hospital, Wuhan, Hubei, China.

出版信息

Arch Physiol Biochem. 2024 Apr;130(2):119-127. doi: 10.1080/13813455.2021.1985144. Epub 2021 Oct 21.

Abstract

Diabetic retinopathy (DR) is the main cause of adult insomnia, which causes certain social and economic pressure. This research was to investigate the role and regulatory mechanisms of MALAT1, miR-378a-3p and PDE6g in retinal microvascular endothelial cells (RMECs) under high glucose (HG). MALAT1, Mir-378a-3p and PDE6G expressions level were detected by qRT-PCR and Western blot. The proliferation, Bax and Bcl-2 protein expression of RMECs were detected by CCK-8 and western blot. The target relationships of MALAT1, miR-378a-3p and PDE6G were determined by bioinformatics analysis, dual-luciferase reporter gene, RIP and RNA pull-down assay. HG enhanced the expression of MALAT1 and PDE6G, and inhibited the expression of miR-378a-3p. Overexpression of MALAT1 promotes the proliferation of RMECs and inhibits apoptosis under HG condition. MALAT1 competitively adsorbed miR-378a-3p, which targeted PDE6G. Data reveal that MALAT1/miR-378a-3p/PDE6G signal axis restrain the apoptosis of RMECs under HG. This finding may help to delay the development of DR.

摘要

糖尿病性视网膜病变 (DR) 是成人失眠的主要原因,会给社会和经济带来一定压力。本研究旨在探讨长链非编码 RNA(lncRNA) MALAT1、miR-378a-3p 和磷酸二酯酶 6G(PDE6G)在高糖 (HG) 环境下对视网膜微血管内皮细胞 (RMECs) 的作用及其调控机制。采用 qRT-PCR 和 Western blot 检测 MALAT1、miR-378a-3p 和 PDE6G 的表达水平,采用 CCK-8 和 Western blot 检测 RMECs 的增殖、Bax 和 Bcl-2 蛋白表达。通过生物信息学分析、双荧光素酶报告基因、RIP 和 RNA 下拉实验确定 MALAT1、miR-378a-3p 和 PDE6G 的靶标关系。HG 增强了 MALAT1 和 PDE6G 的表达,抑制了 miR-378a-3p 的表达。在 HG 条件下,过表达 MALAT1 促进 RMECs 的增殖并抑制细胞凋亡。MALAT1 竞争性吸附 miR-378a-3p,miR-378a-3p 靶向 PDE6G。研究数据表明,MALAT1/miR-378a-3p/PDE6G 信号轴可抑制 HG 下 RMECs 的凋亡。这一发现可能有助于延缓 DR 的发展。

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