title: Overexpression of vasostatin-1 protects hypoxia/reoxygenation injuries in cardiomyocytes-endothelial cells transwell co-culture system.
abstract: Vasostatin-1 (VS-1) plays important roles in myocardial ischemia/reperfusion injury. We have explored the protective effects of VS-1 on cardiomyocytes using cardiomyocyte-endothelial cells Transwell Co-culture System. Cardiomyocytes and rat aortic endothelial cells (RAECs) were prepared from ventricles and thoraco-abdominal aorta of Sprague-Dawley rats. The experiment used cardiomyocytes alone culture group (C) and cardiomyocytes-RAECs co-culture group (T), each with three subgroups: C-Ad-Null, C-Ad-VS-1, C-Hb (Ad-VS-1 + NO scavenger Hb), or T-Ad-Null, T-Ad-VS-1 transfection, T-Hb. After 48 h incubation, all groups were treated with hypoxia for 60 min and then reoxygenated for 120 min. We also investigated endothelial cells-mediated cardiomyocytes protection. RAECs were treated with hypoxia for 30 min and reoxygenated with normal cardiomyocytes for 120 min. The cardiomyocytes apoptosis rate, aspartate aminotransferase (AST) and creatine kinase isozyme MB (CK-MB) were recorded. As expected, cardiomyocytes apoptosis, AST and CK-MB were significantly increased in the T-Ad-Null group than in the C-Ad-Null group. VS transfection significantly reduced these levels. However, apoptosis, AST and CK-MB levels were increased again after Hb treatment, returning to the similar level of the C-Ad-null group in the C-Hb group, but still significantly lower in the T-Hb group compared with the T-Ad-null group. RAEC injury caused cardiomyocyte injury, and VS-1 transfection of the RAEC decreased apoptosis and the levels of AST and CK-MB. The findings suggest that VS-1 exerts protective effects on the cardiomyocytes directly or indirectly by cardiomyocyte-endothelial cells interaction.
authors: Department of Cardiovascular Surgery, Shanghai Jiao Tong University Affiliated First People's Hospital, 100 Haining Road, Shanghai, 200080, P.R. China.
authors: Jian
authors: J
authors: Liu
authors: Dicheng
authors: D
authors: Yang
authors: Sheng
authors: S
authors: Shi
authors: Lei
authors: L
authors: Lin
authors: Mingdi
authors: M
authors: Xiao
authors: Zhongxiang
authors: Z
authors: Yuan
authors: Min
authors: M
authors: Yu
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology; D017209:Apoptosis; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002417:Cattle; D015687:Cell Hypoxia; D002478:Cells, Cultured; D053379:Chromogranin A / Q000235:genetics / Q000378:metabolism*; D018920:Coculture Techniques; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D015870:Gene Expression; D006454:Hemoglobins / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000378:metabolism; D010446:Peptide Fragments / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014162:Transfection
chemical_list: D053379:Chromogranin A; D006454:Hemoglobins; D010446:Peptide Fragments; C064110:vasostatin I; D001219:Aspartate Aminotransferases; D052279:Creatine Kinase, MB Form
keywords: cardiomyocytes; endothelial cells; hypoxia; myocardial damage; transwell co-culture system; vasostatin-1