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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. | 摘要: | 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. |
URI: | http://hdl.handle.net/11455/32576 | ISSN: | 1471-2121 | DOI: | 10.1186/1471-2121-12-19 |
Appears in Collections: | 獸醫學系所 |
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