AGE-BSA down-regulates endothelial connexin43 gap junctions

BMC Cell Biology

Research Article

Chi-Young Wang¹  Hsueh-Hsiao Wang²  Hung-I Yeh²  Ta-Chuan Hung³  Yi-Chun Lin³  Heng-Ju Chen⁴  Hung-Jen Liu⁵ 

[1] Department of Veterinary Medicine, College of Veterinary Medicine, National Chung Hsing University, 250 Road Kuo Kuang, 402, Taichung, TAIWAN;Departments of Internal Medicine and Medical Research, Mackay Memorial Hospital, 45 Road Minsheng, 251, New Taipei City, TAIWAN;Department of Medicine, Mackay Medical College, 46 Road Zhongzheng, 252, New Taipei City, TAIWAN;Departments of Internal Medicine and Medical Research, Mackay Memorial Hospital, 45 Road Minsheng, 251, New Taipei City, TAIWAN;Department of Nursing, Mackay Medicine, Nursing and Management College, 92 Road Shengjing, 112, Taipei, TAIWAN;Graduate Institute of Biotechnology, National Ping-Tung University of Science and Technology, 1 Road Shuefu, 912, Pingtung, TAIWAN;Institute of Molecular Biology, College of Life Sciences, National Chung Hsing University, 250 Road Kuo Kuang, 402, Taichung, TAIWAN;

关键词: SB203580;    PD98059;    Glycated Albumin;    Cx43 Expression;    Human Aortic Endothelial Cell;   

DOI  :  10.1186/1471-2121-12-19

 received in 2010-12-13, accepted in 2011-05-16,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundAdvanced glycation end products generated in the circulation of diabetic patients were reported to affect the function of vascular wall. We examined the effects of advanced glycation end products-bovine serum albumin (AGE-BSA) on endothelial connexin43 (Cx43) expression and gap-junction communication.ResultsIn human aortic endothelial cells (HAEC) treated with a series concentrations of AGE-BSA (0-500 μg/ml) for 24 and 48 hours, Cx43 transcript and Cx43 protein were reduced in a dose dependent manner. In addition, gap-junction communication was reduced. To clarify the mechanisms underlying the down-regulation, MAPKs pathways in HAEC were examined. Both a MEK1 inhibitor (PD98059) and a p38 MAPK inhibitor (SB203580) significantly reversed the reductions of Cx43 mRNA and protein induced by AGE-BSA. Consistently, phosphorylation of ERK and p38 MAPK was enhanced in response to exposure to AGE-BSA. However, all reversions of down-regulated Cx43 by inhibitors did not restore the functional gap-junction communication.ConclusionsAGE-BSA down-regulated Cx43 expression in HAEC, mainly through reduced Cx43 transcription, and the process involved activation of ERK and p38 MAPK.

【 授权许可】

Unknown   
© Wang et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.