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 ...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.展开更多
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).
文摘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.
