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標題: AGE-BSA down-regulates endothelial connexin43 gap junctions
作者: Wang, Chi-Young
Liu, Hung-Jen
Chen, Heng-Ju
Lin, Yi-Chun
Wang, Hsueh-Hsiao
Hung, Ta-Chuan
Yeh, Hung-I
關鍵字: contain multiple connexins;activated protein-kinase;intercellular;communication;phosphorylation status;signaling pathway;epithelial-cells;expression;degradation;dysfunction;pressure
Project: Bmc Cell Biology, Volume 12.
Background: Advanced 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. Results: In human aortic endothelial cells (HAEC) treated with a series concentrations of AGE-BSA (0-500 mu g/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. Conclusions: AGE-BSA down-regulated Cx43 expression in HAEC, mainly through reduced Cx43 transcription, and the process involved activation of ERK and p38 MAPK.
ISSN: 1471-2121
DOI: 10.1186/1471-2121-12-19
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