Abstract
BackgroundMyocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear.Materials and methodsExpression 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.ResultsIn 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.ConclusionTherefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.
Highlights
Myocardial infarction (MI) affects the expression of a large number of Long non-coding RNAs (lncRNAs), while the functions of those dysregulated lncRNAs are mostly unclear
In the present study we explore the involvement of lncRNA MORT in MI and explore its possible interactions with miR-93
MORT and miR-93 expression was altered in mice MI models Expression of MORT and miR-93 in heart tissues and plasma of both MI mice and Sham mice was detected by RT-qPCR
Summary
Myocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear. In spite of the lack of protein products, lncRNAs participate in both physiological and pathological processes through the regulation of downstream genes at multiple levels, such as methylation, posttranscriptional regulation and translational regulation [3, 4]. Both clinical and experimental experiments have revealed that lncRNAs are critical determinants in human diseases [5], and the regulation of lncRNAs expression may contribute to disease treatment [6]. The function of lncRNAs in other diseases is largely unknown. How to prevent and improve treatment of MI is a major task for public
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