Targeting the MicroRNA-490-3p-ATG4B-Autophagy Axis Relieves Myocardial Injury in Ischemia Reperfusion
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ORIGINAL ARTICLE
Targeting the MicroRNA-490-3p-ATG4B-Autophagy Axis Relieves Myocardial Injury in Ischemia Reperfusion Yufu Wu 1 & Qing Mao 2 & Xiulin Liang 3 Received: 16 June 2019 / Accepted: 13 February 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract We investigated the potential role of miR-490-3p in ischemia reperfusion (IR) injury. We first determined the expression of miR490-3p and autophagy-related 4B cysteine (ATG4B) in IR. Then, to explore whether miR-490-3p would affect autophagy, apoptosis, and IR injury, we evaluated apoptosis, autophagy, and infarct size via gain- and loss-of-function experiments. Furthermore, we used adenovirus to enhance or inhibit the expression of ATG4B, and then measured autophagy, apoptosis, and IR injury. miR-490-3p was downregulated in the hearts during the process of IR, while ATG4B was upregulated. The inhibition of miR-490-3p or overexpression of ATG4B could promote the expression of LC3II, increase the autolysosomes, inhibit the expression of p62, and reduce infarct size. On all accounts, the inhibition of miR-490-3p could promote autophagy to reduce myocardial IR injury by upregulating ATG4B, a finding that provides new insights for the protective mechanism of autophagy in IR. Keywords microRNA-490-3p . Autophagy-related 4B cysteine . Autophagy . Apoptosis . Ischemia reperfusion
Introduction Ischemia reperfusion (IR) is a pathological condition caused by the immediate recovery of perfusion of blood after the restricted blood supply to organs [1]. The nature of the injury caused by IR is very complex and influenced by various factors [2], and can lead to significant morbidity and mortality in myocardial infarction and ischemic stroke; in addition, IR injury represents a huge challenge for organ transplantation
Associate Editor Joost Sluijter oversaw the review of this article * Qing Mao [email protected] 1
Department of Cardiology, Liuzhou Traditional Chinese Medical Hospita, The Third Affiliated Hospital of Guangxi University of Chinese Medicine, Liuzhou 545001, People’s Republic of China
2
Department of Cardiology, Nanjing Lishui People’s Hospital, Zhongda Hospital Lishui Branch, Southeast University, No. 86, Chongwen Road, Lishui District, Nanjing 211200, Jiangsu, People’s Republic of China
3
Department of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530007, People’s Republic of China
and cardiothoracic surgery [1]. As a deleterious aspect of myocardial reperfusion injury, reperfusion injury is a deadly myocardial injury aroused by coronary blood flow restoration after an ischemic episode [3]. Myocardial IR injury can cause myocardial cell death (necrosis, apoptosis, and autophagy), myocardial cell hypertrophy, cardiac fibrosis, and impaired angiogenesis [4]. For instance, as an atypical serine/ threonine kinase, mammalian protein kinase or mechanism target rapamycin (mTOR) plays an important role in ischemic injury [5]. Before ischemia, endoplasmic reticulum stress– induced autophagy has b
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