摘要
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 Ca^(2+) 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.
出处
《BIOCELL》
SCIE
2024年第9期1369-1377,共9页
生物细胞(英文)
基金
supported by the National Nature Science Foundation of the People’s Republic of China(No.81400225 for Zulong Sheng and No.82000382 for Yanru He)
the Jiangsu Provincial Medical Youth Talent(No.QNRC2016815).