[No authors listed]
Myocardial infarction (MI) is a severe heart disease caused by acute, persistent ischemia or hypoxia and finally leads to heart failure and sudden death. However, the intrinsic molecular mechanisms of MI remain largely unknown. lncRNAs have also been implicated in the process of ischemic heart diseases. However, the role of lncRNA TTTY15 in MI is not elucidated. We evaluated the expression of TTTY15 in MI and human cardiomyocyte under hypoxia. We explored the role of TTTY15 in cell injury under hypoxia. We searched for potential target of TTTY15. Up-regulation of TTTY15 was associated with hypoxia. Silencing TTTY15 prevented hypoxia-induced cell apoptosis and rescued the cell migration and invasion. TTTY15 targeted miR-455-5p, which regulated the Jun dimerization protein 2 (JDP2) expression. Knocking down miR-455-5p abolished effects of TTTY-15 silencing on cell injury. Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p.
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