Abstract
BackgroundLong noncoding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the development of acute myocardial infarction (AMI). However, the molecular mechanism and biological function of MALAT1 in AMI remained unclear. MethodsThe expression levels of MALAT1, miR-320 and phosphatase and tensin homolog deleted on chromosome 10 (Pten) in a mouse model of AMI and sham-operated mice were determined by quantitative real-time PCR (qRT-PCR) and western blotting, respectively. The relationships between miR-320 and MALAT1, Pten were confirmed by luciferase reporter assay. The roles of MALAT1, miR-320 and Pten in myocardial apoptosis were evaluated using Annexin V-FITC/PI double-labeled flow cytometry. Echocardiographic evaluation, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarct size and myocardial apoptosis using terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were used to examine the impact of MALAT1 on myocardial injury. ResultsMALAT1 and Pten were highly expressed, while miR-320 was suppressed in MI group. Mechanistically, MALAT1 may serve as a sponge for miR-320 to upregulate Pten, a direct target of miR-320. Moreover, MALAT1 knockdown overturned the pro-apoptotic effect of miR-320 in vitro and in vivo. ConclusionMALAT1 knockdown attenuated myocardial apoptosis through suppressing Pten expression by sponging miR-320 in mouse AMI.
Published Version
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