Open Access

ARTICLE

Upregulation of miR-143-3p attenuates oxidative stress-mediated cell ferroptosis in cardiomyocytes with atrial fibrillation by degrading glutamic-oxaloacetic transaminase 1

by Yuan Song^1,#, Cai Wei^2,#, Jingjing Wang^3,*

1 Department of Functional Examination, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, 830000, China
2 Health Care Third Department, Xinjiang Military Region General Hospital, Urumqi, 830000, China
3 Department of Emergency, The People’s Hospital of Suzhou New District, Suzhou, 215000, China

* Address correspondence to: Jingjing Wang,
# These authors contributed equally to this work

BIOCELL 2021, 45(3), 733-744. https://doi.org/10.32604/biocell.2021.013236

Received 30 July 2020; Accepted 22 November 2020; Issue published 03 March 2021

Abstract

Oxidative stress-mediated cell death in cardiomyocytes contributes to the development of atrial fibrillation. However, the detailed mechanisms are still unclear. In the present study, we established atrial fibrillation models in mice. The cardiomyocytes were isolated from atrial fibrillation mice and normal mice and were cultured in vitro, respectively. The results showed that cell proliferation and viability in cardiomyocytes with atrial fibrillation were significantly lower than the cells from the normal mice. Consistently, atrial fibrillation cardiomyocytes were prone to suffer from apoptotic cell death. Also, the oxidative stress and ferroptosis-associated signatures were significantly increased in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes, and ferroptosis inhibitor and NAC rescued cell viability in atrial fibrillation cardiomyocytes during in vitro cell culture. In addition, low-expressed miR- 143-3p was observed in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes, and overexpression of miR-143-3p increased cell proliferation and inhibited cell death in atrial fibrillation cardiomyocytes. Furthermore, glutamic-oxaloacetic transaminase 1 could be negatively regulated by miR-143-3p in normal cardiomyocytes, and miR-143-3p overexpression inhibited cell ferroptosis in atrial fibrillation cardiomyocytes by sponging glutamicoxaloacetic transaminase 1. Collectively, overexpression of miR-143-3p increased cell viability and promoted cell proliferation in cardiomyocytes with atrial fibrillation by inhibiting glutamic-oxaloacetic transaminase 1 mediated oxidative damages and cell ferroptosis.

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