Staphylococcal enterotoxin A modulates intracellular Ca2+ signal pathway in human intestinal epithelial cells
Staphylococcal enterotoxin A modulates intracellular Ca2+ signal pathway in human intestinal epithelial cells
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DOI：
10.1016/j.febslet.2005.07.005
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发表时间：
2005-08-15
期刊：
影响因子：
3.5
通讯作者：
Nakane, A
中科院分区：
文献类型：
--
作者：
Hu, DL;Suga, S;Nakane, A
在此，我们证明了葡萄球菌肠毒素A(SEA)诱导人肠上皮细胞内钙离子([Ca~(2+)](I))增加，[Ca~(2+)](I)从细胞内储备物中释放出来。一氧化氮合酶抑制剂N-G-单甲基-L-精氨酸和胍可明显抑制SEA引起的[Ca~(2+)]_(I)升高。肠上皮细胞在静息状态下表达内皮型一氧化氮合酶，在肿瘤坏死因子-α刺激后表达诱导型一氧化氮合酶。经肿瘤坏死因子-α处理的细胞内[Ca~(2+)]_(I)显著升高，并被一氧化氮合酶抑制剂抑制。这些结果表明，SEA调节的[Ca~(2+)](I)信号依赖于人肠上皮细胞中NOS的表达。(C)2005年，由Elsevier B.V.代表欧洲生化学会联合会出版。
We demonstrate here that staphylococcal enterotoxin A (SEA) induces an increase in intracellular calcium ([Ca2+](i)) in human intestinal epithelial cells and the [Ca2+](i) is released from intracellular stores. SEA-induced increase of [Ca2+](i) was clearly inhibited by treatment with a nitric oxide synthase (NOS) inhibitors, N-G-monomethyl-L-arginine and guanidine. Intestinal epithelial cells express endothelial NOS in resting cell condition, and express inducible NOS after stimulating with tumor necrosis factor (TNF)-alpha. TNF-alpha-pretreated cells showed a significant increase in [Ca2+](i) that was also inhibited by the NOS inhibitor. These results suggest that SEA modulated [Ca2+](i) signal is dependent on NOS expression in human intestinal epithelial cells. (c) 2005 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.