کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3416961 | 1225166 | 2009 | 5 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Role of calcium/calmodulin signaling pathway in Vibrio vulnificus cytolysin-induced hyperpermeability Role of calcium/calmodulin signaling pathway in Vibrio vulnificus cytolysin-induced hyperpermeability](/preview/png/3416961.png)
Endothelial hyperpermeability, a hallmark of septicemia, is induced by stress fiber formation, which is primarily regulated by the calcium/calmodulin signaling pathway in endothelial cells. We previously reported that trifluoperazine, a calcium/calmodulin antagonist, blocks Vibrio vulnificus cytolysin (VVC) -induced lethality at in vivo animal model. The object of this study was therefore to examine whether VVC induces stress fiber formation through calcium/calmodulin signaling in endothelial cells. Here, we monitored calcium-influx after treatment of VVC using confocal microscopy in CPAE cells, pulmonary endothelial cell line. Interestingly, we found that VVC-induced dose-dependently increases of [Ca2+]i in CPAE cells. Moreover, VVC-induced stress fiber formation as well as phosphorylation of myosin light chain (MLC) in a dose- and time-dependent manner, which was completely blocked by trifluoperazine. These results suggest that the calcium/calmodulin signaling pathway plays a pivotal role in VVC-induced hyperpermeability.
Journal: Microbial Pathogenesis - Volume 47, Issue 1, July 2009, Pages 47–51