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- Title
MiR-219a-5p exerts a protective function in a mouse model of myocardial infarction.
- Authors
SHENG, ZULONG; HE, YANRU; CAI, JUNYAN; JI, YUQIN; YAO, YUYU; MA, GENSHAN
- 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.
- Subjects
LABORATORY mice; PEARSON correlation (Statistics); ANIMAL disease models; ENZYME-linked immunosorbent assay; TETRAZOLIUM chloride; MYOCARDIAL infarction; INFARCTION; GENE amplification
- Publication
Biocell, 2024, Vol 48, Issue 9, p1369
- ISSN
0327-9545
- Publication type
Article
- DOI
10.32604/biocell.2024.049905