Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Abstract

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 dualluciferase 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 OGDevoked 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-132mimic-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.

MicroRNA-132 attenuated cardiac fibrosis in myocardial infarction-induced heart failure rats

“…It showed that miR-132 inhibits cardiomyocyte apoptosis, and ameliorates myocardial remodeling in rats with MI through IL-1β down-regulation [ 35 ]. miR-132 exhibited the protective impacts on H9C2 cells against oxygen and glucose deprivation-induced injury via targeting FOXO3A [ 36 ]. Our present study found that miR-132 targeted PTEN in CFs, which is supported by previous study [ 22 ].…”

Circular RNA _NLRP1 targets mouse microRNA-199b-3p to regulate apoptosis and pyroptosis of hippocampal neuron under oxygen-glucose deprivation exposure

“…Primary neurons of the CA1 hippocampus from E12-E14 embryos of C57BL/6 J mice were isolated, and CA1 hippocampal neurons were seeded into serum-free neuron basal culture medium containing 2% B27 supplement and 2 mM glutamine. On day 8 in vitro, neurons were induced with OGD [ 16 ]. Hippocampal neuronal cells were cultured in medium containing no glucose in incubator with 94% N 2 , 5% CO 2 and 1% O 2 .…”

Advances in miR-132-Based Biomarker and Therapeutic Potential in the Cardiovascular System

“…It is well demonstrated that miR-132/212 plays an anti-apoptotic role by activating the phosphatidylinositol-3 kinase/protein kinase B pathway in cardiomyocytes ( Ucar et al, 2012 ). Overexpression of miR-132 in cardiomyocytes in vitro contributes to enhanced resistance to hypoxia, hydrogen peroxide, and hypoxia and glucose deprivation-induced cell death ( Liu et al, 2018a ; Lei et al, 2020a ; Zhang et al, 2020 ). Besides, in vivo studies have shown that miR-132 was downregulated in cardiomyocytes from MI rats compared to sham-operated rats, and overexpression of miR-132 mitigated cardiomyocyte apoptosis and myocardial remodeling, and this effect may be achieved in part through inhibition of interleukin-1β ( Zhao et al, 2020 ).…”