Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes
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Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes Fang Wu 1,2,3 & Feng Wang 1,2 & Qian Yang 1,2 & Yawen Zhang 1,2 & Ke Cai 2 & Lian Liu 2 & Shuchun Li 4 & YuanZheng Zheng 2 & Jialing Zhang 2 & Yiting Gui 1,2 & Youhua Wang 5 & Xu Wang 6 & Yonghao Gui 2 & Qiang Li 1 Received: 7 August 2020 / Accepted: 30 September 2020 / Editor: Tetsuji Okamoto # The Author(s) 2020
Abstract Maternal hyperglycemia potentially inhibits the development of the fetal heart by suppressing cardiomyocyte proliferation and promoting apoptosis. Different studies have indicated that miRNAs are key regulators of cardiomyocyte proliferation, differentiation, and apoptosis and play a protective role in a variety of cardiovascular diseases. However, the biological function of miRNA-23a in hyperglycemia-related cardiomyocyte injury is not fully understood. The present study investigated the effect of miRNA-23a-3p on cell proliferation and apoptosis in a myocardial injury model induced by high glucose. H9c2 cardiomyocytes were exposed to high glucose to establish an in vitro myocardial injury model and then transfected with miRNA-23a-3p mimics. After miRNA-23a-3p transfection, lens-free microscopy was used to dynamically monitor cell numbers and confluence and calculate the cell cycle duration. CCK-8 and EdU incorporation assays were performed to detect cell proliferation. Flow cytometry was used to measured cell apoptosis. Upregulation of miRNA-23a-3p significantly alleviated high glucose-induced cell apoptosis and cell proliferation inhibition (p < 0.01 and p < 0.0001, respectively). The cell cycle of the miRNA-23a-3p mimics group was significantly shorter than that of the negative control group (p < 0.01). The expression of cell cycle– activating and apoptosis inhibition-associated factors Ccna2, Ccne1, and Bcl-2 was downregulated by high glucose and upregulated by miRNA-23a-3p overexpression in high glucose-injured H9c2 cells. miRNA-23a-3p mimics transfection before high glucose treatment had a significantly greater benefit than transfection after high glucose treatment (p < 0.0001), and the rescue effect of miRNA-23a-3p increased as the concentration increased. This study suggests that miRNA-23a-3p exerted a dose- and time-dependent protective effect on high glucose-induced H9c2 cardiomyocyte injury. Keywords miRNA-23a-3p . Myocardial injury . Hyperglycemia . H9c2 . Proliferation . Apoptosis
* Yonghao Gui [email protected] * Qiang Li [email protected] 1
Translational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children’s Hospital of Fudan University, Shanghai 201102, China
2
Cardiovascular Center, Children’s Hospital of Fudan University, Shanghai 201102, China
3
Department of Neonatology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China
4
Department of Emergency, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, Chin
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