@Article{biocell.2024.049905,
AUTHOR = {ZULONG SHENG, YANRU HE, JUNYAN CAI, YUQIN JI, YUYU YAO, GENSHAN MA},
TITLE = {MiR-219a-5p exerts a protective function in a mouse model of myocardial infarction},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {9},
PAGES = {1369--1377},
URL = {http://www.techscience.com/biocell/v48n9/57807},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> 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. <b>Methods:</b> 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 Ca<sup>2+</sup> transporting 2 (ATP2A2), the luciferase activity assay and Pearson’s correlation analysis were employed. <b>Results:</b> 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. <b>Conclusion:</b> In a mouse model of MI, miR-219a-5p exerted a potent protective effect via direct targeting of ATP2A2.},
DOI = {10.32604/biocell.2024.049905}
}