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Long noncoding RNA AK088388 regulates autophagy through miR‐30a to affect cardiomyocyte injury
Author(s) -
Wang Jingjing,
Bie Zidong,
Sun Chaofeng
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28300
Subject(s) - autophagy , downregulation and upregulation , microbiology and biotechnology , microrna , reperfusion injury , apoptosis , small interfering rna , luciferase , biology , rna , chemistry , ischemia , cell culture , medicine , transfection , biochemistry , gene , genetics
Finding ways to reduce myocardial ischemia/reperfusion injury in the process of myocardial infarction has been an area of intense study in the field of heart disease. Recent studies have shown that long noncoding RNA (lncRNA) and autophagy play important roles in cardiovascular diseases. In our study, software analysis and dual‐luciferase reporter assays have shown that miR‐30a has binding sites on both AK088388 and Beclin‐1. Continuing experiments found that miR‐30a expression is downregulated, while the expressions of AK088388, Beclin‐1, and LC3‐II are upregulated in hypoxia/reoxygenation (H/R) cardiomyocytes; miR‐30a inhibits the expression of AK088388, Beclin‐1, and LC3‐II in H/R cardiomyocytes, while AK088388 promotes the expression of Beclin‐1 and LC3‐II and inhibits miR‐30a expression. AK088388 small interfering RNA and miR‐30a mimics can promote the viability of H/R cardiomyocytes, reduce lactate dehydrogenase release, and reduce apoptosis. Mutations of the miR‐30a binding site in AK088388 could not block the effects of miR‐30a mentioned above. Therefore, AK088388 can competitively bind to miR‐30a, promoting the expression of Beclin‐1 and LC3‐II, autophagy, and eventually cell damage. This finding provides new evidence for understanding the role of lncRNA in myocardial ischemia/reperfusion injury.