Open Access

ARTICLE

MiR-219a-5p exerts a protective function in a mouse model of myocardial infarction

ZULONG SHENG^*, YANRU HE, JUNYAN CAI, YUQIN JI, YUYU YAO, GENSHAN MA

Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, 210009, China

* Corresponding Author: ZULONG SHENG. Email:

BIOCELL 2024, 48(9), 1369-1377. https://doi.org/10.32604/biocell.2024.049905

Received 22 January 2024; Accepted 20 July 2024; Issue published 04 September 2024

Abstract

Background: Myocardial infarction (MI) is known worldwide for its important disabling features, including myocarditis and cardiomyocyte apoptosis. It is believed that microRNA (miRNA) has a role in the cellular processes of apoptosis and myocarditis, and miR-219a-5p has been found to suppress the inflammatory response. However, unknown is the precise mechanism by which miR-219a-5p contributes to MI. Methods: We measured the expression of miR-219a-5p and evaluated its effects on target proteins, inflammatory factors, and apoptosis in a mouse model of MI. Echocardiography was utilized to examine the MI clinical index, and triphenyl tetrazolium chloride staining was employed to analyze the infarcted region. Enzyme-linked immunosorbent assay and Western blotting measured serum and molecular markers in heart tissues. To quantify the association with miR-219a-5p and ATPase sarcoplasmic/endoplasmic reticulum Ca²⁺ transporting 2 (ATP2A2), the luciferase activity assay and Pearson’s correlation analysis were employed. Results: MiR-219a-5p exhibited low expression in a mouse model of MI, and its amplification prevented both apoptotic and inflammatory reactions. Specifically, miR-219a-5p targeted ATP2A2. Conclusion: In a mouse model of MI, miR-219a-5p exerted a potent protective effect via direct targeting of ATP2A2.

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