LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

• DOI: 10.1002/jcp.27925
• Publication Date: 2018-12-08T05:28:24Z
• Authors: Xiaoyan Guo; Xiaoguang Wu; Yan Han; Erhu Tian; Jiangtao Cheng
• Keywords: MALAT1; Viability assay; ULK1

Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate proliferation metastasis several tumors. However, little is known about effects MALAT1 in MI regulating cell date after MI. In our study, first, it was shown that expression levels were increased samples compared with normal tissues using quantitative reverse-transcription polymerase chain reaction. Then, knockdown could significantly decrease viability increase apoptotic rates isoproterenol (ISO)-treated H9C2 cells. addition, we screened possible target found miR-558 its direct dual luciferase reporter assay, indicating functioned as decoys sponging miR-558. Transfection mimic decreased enhanced apoptosis. Furthermore, revealed downregulate ULK1 suppressed ISO-induced protective autophagy. Activation MALAT1/miR-558/ULK1 pathway protected cells from mitochondria-dependent Finally, used MALAT1-knockout mice further cardiomyocytes apoptosis partially improved cardiac functions upon ISO treatment. conclusion, elucidated lncRNA by thus promoting ULK1-dependent Targeting might become a potential strategy protecting during