Role of lncRNA‐MEG8/miR‐296‐3p axis in gestational diabetes mellitus

活力测定 妊娠期糖尿病 细胞凋亡 医学 MTT法 胰岛素 细胞 流式细胞术 下调和上调 实时聚合酶链反应 糖尿病 污渍 癌症研究 内分泌学 生物 妊娠期 怀孕 基因 免疫学 生物化学 遗传学
作者
Guiping Bian,Yanchun Xue,Yinmei Liu,Yan Xu,Guifen Chen,Huiping Wu
出处
期刊:Nephrology [Wiley]
卷期号:27 (12): 994-1002 被引量:6
标识
DOI:10.1111/nep.14112
摘要

Gestational diabetes mellitus (GDM) is the most common complication in pregnancy. This study aimed to investigate the potential mechanism and effects of long-noncoding RNA maternally expressed 8 (lncRNA-MEG8) in GDM.Targeted interactions involving lncRNA-MEG8 and miR-296-3p were initially predicted using starBase software and then confirmed using dual-luciferase reporter gene analysis. The expression levels of lncRNA-MEG8 and miR-296-3p in peripheral blood samples from patients with GDM were measured using reverse transcription-quantitative polymerase chain reaction. Enzyme-linked immunosorbent assay was used to evaluate the overall levels of insulin and insulin secretion. Additionally, MTT and flow cytometric methods were used to detect cell viability and apoptosis. Cell apoptosis-associated proteins were determined by western blotting.Our results indicated that lncRNA-MEG8 is a potential target of miR-296-3p. lncRNA-MEG8 level was higher, whereas that of miR-296-3p was lower in patients with GDM than in healthy individuals. LncRNA-MEG8-siRNA promoted insulin content and secretion. Furthermore, MEG8-siRNA increased cell viability and decreased apoptosis. However, these changes were reversed by an miR-296-3p inhibitor. Moreover, a miR-296-3p mimic had the same effect on INS-1 cells as MEG8-siRNA, as evidenced by enhanced insulin secretion, cell viability, and reduced apoptosis.LncRNA-MEG8-siRNA promotes pancreatic β-cell function by upregulating miR-296-3p.
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