lncRNA MALAT1通过miR-378a-3p上调PDE6G促进糖尿病视网膜病变。

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-04-01 Epub Date: 2021-10-21 DOI:10.1080/13813455.2021.1985144

Xiaoxia Li

{"title":"lncRNA MALAT1通过miR-378a-3p上调PDE6G促进糖尿病视网膜病变。","authors":"Xiaoxia Li","doi":"10.1080/13813455.2021.1985144","DOIUrl":null,"url":null,"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.","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"lncRNA MALAT1 promotes diabetic retinopathy by upregulating PDE6G via miR-378a-3p.\",\"authors\":\"Xiaoxia Li\",\"doi\":\"10.1080/13813455.2021.1985144\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":8331,\"journal\":{\"name\":\"Archives of Physiology and Biochemistry\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of Physiology and Biochemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/13813455.2021.1985144\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/10/21 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Physiology and Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2021.1985144","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/10/21 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}

引用次数: 0

摘要

糖尿病视网膜病变（DR）是导致成人失眠的主要原因，给社会和经济造成一定压力。本研究旨在探讨MALAT1、miR-378a-3p和PDE6g在高糖条件下视网膜微血管内皮细胞（RMECs）中的作用和调控机制。通过qRT-PCR和Western blot检测MALAT1、Mir-378a-3p和PDE6G的表达水平。CCK-8和Western blot检测了RMECs的增殖、Bax和Bcl-2蛋白的表达。通过生物信息学分析、双荧光素酶报告基因、RIP和RNA pull-down实验确定了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 可促进 RMECs 的增殖并抑制细胞凋亡。MALAT1能竞争性吸附miR-378a-3p，从而靶向PDE6G。数据显示，MALAT1/miR-378a-3p/PDE6G 信号轴抑制了 HG 条件下 RMECs 的凋亡。这一发现可能有助于延缓DR的发展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

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

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.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.