Long noncoding RNA AK088388 regulates autophagy through miR-30a to affect cardiomyocyte injury |
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Authors: | Jing-jing Wang Zi-dong Bie Chao-feng Sun |
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Affiliation: | 1. Department of Medicine, Xi’an Jiaotong University, Xi’an, Shanxi, China Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China;2. Department of Cardiology, Yantai Yuhuangding Hospital, Yantai, Shandong, China;3. Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shanxi, China |
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Abstract: | 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. |
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Keywords: | autophagy cardiomyocyte long noncoding RNA (lncRNA) miR-30a myocardial infarction |
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