Protective effect of HDL on NADPH oxidase-derived super oxide anion mediates hypoxia-induced cardiomyocyte apoptosis

doi:10.1371/journal.pone.0179492

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Title:	Protective effect of HDL on NADPH oxidase-derived super oxide anion mediates hypoxia-induced cardiomyocyte apoptosis
Authors:	Wen, Su-Ying Tamilselvi, Shanmugam Shen, Chia-Yao Day, Cecilia Hsuan Chun, Li-Chin Cheng, Li-Yi Ou, Hsiu-Chung Chen, Ray-Jade Viswanadha, Vijaya Padma Kuo, Wei-Wen Huang, Chih-Yang
Contributors:	Taipei City Hosp, Renai Branch, Dept Dermatol Mackay Jr Coll Med Nursing & Management, Ctr Gen Educ China Med Univ, Grad Inst Basic Med Sci MeiHo Univ, Dept Nursing Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm Asia Univ, Dept Biol Sci & Technol Taipei Med Univ, Dept Surg, Sch Med, Coll Med Bharathiar Univ, Dept Biotechnol, Coimbatore China Med Univ, Dept Biol Sci & Technol China Med Univ, Grad Inst Chinese Med Sci
Keywords:	Serum Response Factor N-Terminal Kinases Neutrophil Respiratory Burst Activated Protein-Kinases Oxidative Stress Heart-Failure Cardiovascular-Disease Gene-Expression Hif-1-Alpha Angiogenesis
Date:	2017-06-15
Issue Date:	2018-11-30 15:55:47 (UTC+8)
Publisher:	Public Library Science
Abstract:	Cardiovascular diseases are the leading cause of death of death in Taiwan. Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death. Coronary heart disease (CHD) occurs when plaque builds up in the coronary arteries to cause the ischemic heart disease which will enhance myocardial remodeling and also induce myocardial hypoxia. High density lipoprotein (HDL) has been proposed to have cardio-protective effects. Under hypoxic conditions (1%O-2 for 24hr), in H9c2 cells, reactive oxygen species (ROS) is induced which leads to cardiomyocyte apoptosis and cardiac dysfunction. Therefore, the present study described the protective effect of HDL on hypoxia-induced cardiomyocyte damage. We investigated the NADPH oxidase-produced ROS-related signaling pathways and apoptosis in cardiomyocytes under hypoxia conditions. Results showed that the ROS mediated cardiac damage might occur via AT1 and PKC activation. Furthermore, hypoxia downregulated the survival protein (p-AKT(ser473)) and anti-apoptotic protein (BCL2), whereas pro-apoptotic protein, Bax and caspase 3 were upregulated. These detrimental effects by ROS and apoptosis were prevented by HDL pretreatment. Our findings revealed the underlying molecular mechanism by which HDL suppresses the hypoxia-induced cardiomyocyte dysfunction. Further, we elucidated the role of HDL on preventing hypoxia induced cardiomyocyte apoptosis is mediated through the inhibition of NADPH oxidase-derived ROS.
Relation:	Plos One, v.12, n.6, e0179492
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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