LncRNA-HOTAIR/MiR-217/GPD2轴治疗心肌细胞缺氧损伤

Pub Date : 2022-02-12 DOI:10.31901/24566330.2022/22.02.808

L. Dai

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引用次数: 0

摘要

本研究检测了lncRNA HOX转录反义RNA (HOTAIR)、miR-217和甘油-3-磷酸脱氢酶2 (GPD2)对缺氧损伤后心肌细胞进展的影响。缺氧处理导致细胞活力降低，细胞凋亡增加。RT-qPCR检测lncRNA HOTAIR的抑制表达。lncRNA HOTAIR过表达可促进AC16细胞活力，抑制细胞凋亡和促炎蛋白表达，而HOTAIR过表达则相反。然后检测MiR-217被HOTAIR过表达抑制，其上调降低AC16细胞活力，促进细胞凋亡和促炎蛋白的表达。荧光素酶报告基因检测证实GPD2被miR-217结合并降低，促进AC16细胞活力，但过表达后抑制细胞凋亡和促炎蛋白的表达。此外，过表达GPD2可激活PI3K/AKT信号通路

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LncRNA HOTAIR/MiR-217/GPD2 Axis Medicates Hypoxia Injury of Myocardial Cells

This study examined impacts of lncRNA HOX Transcript Antisense RNA (HOTAIR), miR-217 and Glycerol-3-phosphate dehydrogenase 2 (GPD2) on progressions of cardiomyocytes after hypoxia damage. Hypoxia treatment induced low cell viability and increased apoptosis. RT-qPCR evaluated suppressed expressions of lncRNA HOTAIR. Overexpressed lncRNA HOTAIR accelerated AC16 cell viability but restrained cell apoptosis and proinflammatory protein expressions while the knockdown of HOTAIR caused opposite results. MiR-217 then was examined to be inhibited by HOTAIR overexpression, whose upregulation reduced AC16 cell viability but facilitated apoptosis and pro-inflammatory protein expressions. Luciferase reporter test then verified that GPD2 was bound and decreased by miR-217, which promoted AC16 cell viability but hampered cell apoptosis and pro-inflammatory protein expressions after overexpression. Moreover, PI3K/AKT signaling pathway was activated by overexpression of GPD2

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