LncRNA AZIN1-AS1 ameliorates myocardial ischemia--reperfusion injury by targeting miR-6838-5p/WNT3A axis to activate Wnt-[beta]/catenin signaling pathway.

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Publisher: Springer
Document Type: Report; Brief article
Length: 285 words

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Keywords: LncRNA AZIN1-AS1; Myocardial I/R injury; H/R injury; miR-6838-5p; Wnt-[beta]/catenin signaling pathway Abstract Myocardial reperfusion, the effective therapy for acute myocardial infarction (AMI), commonly leads to myocardial ischemia/reperfusion (I/R) injury. The effects and functional mechanisms of LncRNA AZIN1-AS1 on myocardial I/R injury in vivo and vitro are not uncovered. In our present study, we established myocardial I/R injury model of mice and H/R injury model of cardiomyocytes and we discovered AZIN1-AS1 was decreased but miR-6838-5p was increased significantly in myocardial tissues injured by I/R treatment and H9c2 cells injured by hypoxia/reoxygenation (H/R) treatment. Silencing AZIN1-AS1 down-regulated cell viability but up-regulated apoptosis rate and CK-MB in addition LDH release of cardiomyocyte under H/R injury. However, overexpression of AZIN1-AS1 recovered abovementioned effects. Additionally, miR-6838-5p was found to be the direct target of AZIN1-AS1 and exhibited negative correlation with AZIN1-AS1. Moreover, miR-6838-5p inhibitor effectively eliminated the effects of AZIN1-AS1 knockdown on H/R-injured myocardial cells. Further experiments showed that WNT3A was the target of miR-6838-5p axis and overexpression of WNT3A also counteracted the roles of AZIN1-AS1 knockdown. Furthermore, knockdown of AZIN1-AS1 dramatically inhibited the activity of WNT-[beta]/catenin signaling pathway, which was recovered effectively by plasmid with overexpressing WNT3A. Therefore, this study firstly revealed that LncRNA AZIN1-AS1/miR-6838 axis inhibited apoptosis by activating WNT/[beta]-catenin pathway to protect mice or H9c2 cell from I/R-induced or H/R-induced injury respectively, which advised that AZIN1-AS1 could be regarded as a potential target for treating patients with AMI. Author Affiliation: (1) Emergency Department, Xiamen Cardiovascular Hospital, Xiamen University, Xiamen, China (2) Ultrasonic Department, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999 Jinshan Road, Huli District, 361009, Xiamen, Fujian Province, China (g) m536301900@163.com Article History: Registration Date: 01/04/2022 Received Date: 07/30/2021 Accepted Date: 12/23/2021 Online Date: 01/21/2022 Byline:

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Gale Document Number: GALE|A691177528