Capsaicin induces cofilin dephosphorylation in human intestinal cells: The triggering role of cofilin in tight-junction signaling
Capsaicin induces cofilin dephosphorylation in human intestinal cells: The triggering role of cofilin in tight-junction signaling
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DOI：
10.1016/j.bbrc.2007.02.002
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发表时间：
2007-04-06
影响因子：
3.1
通讯作者：
Tanaka, Toshiyuki
中科院分区：
文献类型：
--
作者：
Nagumo, Yoko;Han, Junkyu;Tanaka, Toshiyuki
Previously, we demonstrated that capsaicin induces tight-junction (TJ) opening in human intestinal Caco-2 cells. In order to clarify the mechanism underlying the TJ opening action of capsaicin, we performed a proteomics study on capsaicin-treated Caco-2 cells. Phosphorylated cofilin was decreased significantly by capsaicin treatment. In addition, capsaicin induced Ca2+ influx in Caco-2 cells and there was a clear correlation between Ca2+ influx and cofilin dephosphorylation (activation). The Ca2+-chelating reagent EGTA blocked the cofilin dephosphorylation induced by both capsaicin and ionomycin, suggesting that the dephosphorylation was mediated by Ca2+ influx. Finally, transepithelial electrical resistance measurements showed that TJ opening accompanied cofilin dephosphorylation. Our data suggest that TJ opening is mediated by cofilin dephosphorylation, which is caused by capsaicin stimuli, including Ca2+ influx. This is the first report of capsaicin action via the dephosphorylation of cofilin in human intestinal cells. (c) 2007 Elsevier Inc. All rights reserved.
