RETRACTED: MicroRNA-132 protects H9c2 cells against oxygen and glucose deprivation-evoked injury by targeting FOXO3A (Retracted article. See vol. 236, pg. 8263, 2021)

被引:13
|
作者
Zhang, Jingze [1 ]
Xu, Haiming [2 ]
Gong, Licheng [2 ]
Liu, Long [2 ]
机构
[1] Second Hosp Jilin Univ, Dept Neurosurg, Changchun, Jilin, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Cardiol, 126 Xiantai Rd, Changchun 130033, Jilin, Peoples R China
关键词
cell apoptosis; FOXO3A; microRNA-132; MIRI; oxygen and glucose deprivation; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; ISCHEMIA-REPERFUSION INJURY; ATTENUATES OXIDATIVE STRESS; CARDIOMYOCYTE APOPTOSIS; MIR-132; CONTRIBUTES; INHIBITION; EXPRESSION; PATHWAY; CANCER;
D O I
10.1002/jcp.28956
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Myocardial ischemia/reperfusion injury (MIRI) is a clinically familiar disease, which possesses a great negative impact on human health. But, the effective treatment is still absent. MicroRNAs (miRNAs) have been testified to play a momentous role in MIRI. The purpose of the study aimed to probe the functions of miR-132 in oxygen and glucose deprivation (OGD)-evoked injury in H9c2 cells. miR-132 expression in H9c2 cells accompanied by OGD disposition was evaluated via real-time quantitative polymerase chain reaction. After miR-132 mimic and inhibitor transfections, the impacts of miR-132 on OGD-affected H9c2 cell viability, apoptosis, cell cycle, and the interrelated factors were appraised by exploiting cell counting kit-8, flow cytometry, and western blot analysis. FOXO3A expression was estimated in above-transfected cells, meanwhile, the correlation between miR-132 and FOXO3A was probed by dual-luciferase report assay. Ultimately, above mentioned cell processes were reassessed in H9c2 cells after preprocessing OGD administration and transfection with si-FOXO3A and si-NC plasmids. We got that OGD disposition obviously enhanced miR-132 expression in H9c2 cells. Overexpressed miR-132 evidently reversed OGD-evoked cell viability repression and apoptosis induction in H9c2 cells. In addition, overexpressed miR-132 mitigated OGD-evoked G0/G1 cell arrest by mediating p21, p27, and cyclin D1 expression. Repression of FOXO3A was observed in miR-132 mimic-transfected cells, which was also predicated as a direct gene of miR-132. We discovered that silenced FOXO3A alleviated OGD-evoked cell injury in H9c2 cells via facilitating cell viability, hindering apoptosis and restraining cell arrest at G0/G1 phase. In conclusion, these investigations corroborated that miR-132 exhibited the protective impacts on H9c2 cells against OGD-evoked injury via targeting FOXO3A.
引用
收藏
页码:176 / 184
页数:9
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