{"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":"<p><p>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.</p>","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}
引用次数: 0
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.
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.