Downregulation of RACK1 is associated with cardiomyocyte apoptosis after myocardial ischemia/reperfusion injury in adult rats

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Date: Mar. 2016
Publisher: Springer
Document Type: Report
Length: 374 words

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Abstract :

To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s11626-015-9981-0 Byline: Long Qian (1,4), Jiahai Shi (1,4), Chi Zhang (2,4), Jiawei Lu (1,4), Xiaoning Lu (1,4), Kunpeng Wu (1,4), Chen Yang (1,4), Daliang Yan (1,4), Chao Zhang (2,4), Qingsheng You (1,4), Xiaojuan Liu (3,4) Keywords: Myocardial ischemia/reperfusion; Apoptosis; RACK1; Rats Abstract: The receptor for activated C kinase 1 (RACK1) is a multifaceted scaffolding protein that mediates the shuttling of activated protein kinase C (PKC) to cellular membranes. In addition, RACK1 could decrease cell apoptosis in a variety of disease models. However, the function of RACK1 in cardiomyocyte apoptosis after myocardial ischemia/reperfusion (I/R) is unknown. In this study, male Sprague--Dawley rats were anesthetized and subjected to myocardial I/R insult consisting of 30 min left anterior descending coronary artery (LAD) occlusion followed by reperfusion for 1, 2, 4, 6, 8, 12, and 24 h. The expression of RACK1 was decreased after myocardial I/R and was associated with cardiomyocyte apoptosis. To further verify the relationship between RACK1 and cardiomyocyte apoptosis, H9c2 cardiomyocytes were cultured under hypoxia for 6 h, then maintained in the regular incubator to reoxygenation. After H9c2 cells were transfected with Flag-RACK1 to overexpress RACK1, RACK1 expression was upregulated in hypoxia/reoxygenation (H/R) 4 h group accompanied with the decrease of cleaved caspase-3 and the increase of Bcl-2 expression. Terminal transferase-mediated biotin dUTP nick end labeling (TUNEL) assay showed that RACK1 overexpression inhibited H9c2 cell apoptosis induced by H/R treatment. Our data suggested that RACK1 might suppress cardiomyocyte apoptosis after I/R, providing a novel molecular target for the therapy of ischemia heart disease. Author Affiliation: (1) Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, People's Republic of China (2) Department of Vasculocardiology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, People's Republic of China (3) Department of Pathogen Biology, Medical College, Nantong University, Nantong, Jiangsu, 226001, People's Republic of China (4) Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College, Nantong University, Nantong, Jiangsu, 226001, People's Republic of China Article History: Registration Date: 09/11/2015 Received Date: 22/08/2015 Accepted Date: 09/11/2015 Online Date: 10/12/2015 Article note: Editor: Tetsuji Okamoto Long Qian, Jiahai Shi, Qingsheng You and Xiaojuan Liu contributed equally to this work.

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Gale Document Number: GALE|A449673652