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Your search keyword '"Li, Rui-Bei"' showing total 2 results
2 results on '"Li, Rui-Bei"'

2. LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.

Author

Liu CY, Zhang YH, Li RB, Zhou LY, An T, Zhang RC, Zhai M, Huang Y, Yan KW, Dong YH, Ponnusamy M, Shan C, Xu S, Wang Q, Zhang YH, Zhang J, and Wang K

Subjects
Animals, Animals, Newborn, Cells, Cultured, Mice, Myocardial Infarction pathology, Myocardial Reperfusion Injury genetics, Myocardial Reperfusion Injury metabolism, Myocytes, Cardiac metabolism, Nuclear Proteins metabolism, Protein Binding, RNA Interference, RNA, Long Noncoding metabolism, Trans-Activators metabolism, Tumor Suppressor Protein p53 metabolism, Autophagy genetics, Myocardial Infarction genetics, Nuclear Proteins genetics, RNA, Long Noncoding genetics, Trans-Activators genetics, Transcriptional Activation, Tumor Suppressor Protein p53 genetics
Abstract

Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H 2 O 2 and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.

Published
2018
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