Background: Myocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear.
Materials and methods: Expression of MORT and miR-93 in hearth tissues and plasma of both MI mice and Sham mice and both MI patients and healthy controls was detected by RT-qPCR. Correlations of expression levels of MORT and miR-93 between hear tissues and plasma of MI mice were explored by performing linear regression.
Results: In the present study we found that MORT expression levels were higher, while expression levels of miR-93 were lower in both plasma and heart tissues of mice MI mice models compared with Sham mice. Plasma levels of MORT and miR-93 were largely consistent with expression levels of MORT and miR-93 in heart tissue of MI mice. MORT expression levels were also higher, while levels of miR-93 were also lower in plasma of MI patients compared with healthy controls. MORT and miR-93 were inversely correlated in MI patients but not in healthy controls. MORT overexpression resulted in inhibited miR-93 expression in cardiomyocytes (AC16 cell line), while miR-93 overexpression did not significantly affect MORT expression. MORT overexpression promoted cardiomyocyte apoptosis, while miR-93 overexpression played and opposite role and attenuated the effects of MORT overexpression.
Conclusion: Therefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.
Keywords: Apoptosis; Cardiomyocyte; Myocardial infarction; lncRNA MORT; miR-93.