Extracellular alkalosis activates ERK mitogen-activated protein kinase of vascular smooth muscle cells through NADPH-mediated formation of reactive oxygen species
摘要：Abstract Extracellular alkalosis induced phosphorylation of extracellular signal-regulated kinase (ERK) and enhanced serum-induced ERK phosphorylation in cultured rat aortic smooth muscle cells. While extracellular alkalinization increased verapamil-sensitive 45Ca2+ uptake into the cells, ERK phosphorylation induced by extracellular alkalosis was not affected by verapamil. On the other hand, probes for oxidant signaling, such as superoxide dismutase, 4,5-dihydroxy-1,3-benzene-disulfonic acid, a cell-permeable antioxidant, and diphenyliodonium, a NADPH oxidase inhibitor, inhibited extracellular alkalosis-induced phosphorylation of ERK. These results suggest that activation of ERK induced by extracellular alkalosis is not dependent on transplasmalemmal Ca2+ entry but is caused by reactive oxygen species derived from an activation of NADPH oxidase.
关键词：Alkalosis; Mitogen-activated protein kinase; Ca2+ channel; Vascular smooth muscle; NADPH oxidase; Oxygen stress; DMEM, Dulbecco’s modified Eagle’s medium; DPI, diphenyliodonium; ERK, extracellular signal-regulated kinase; FBS, fetal bovine serum; PBS, phosphate-buffered saline; PMA, phorbol 12-myristate 13-acetate; SOD, superoxide dismutase; VDCC, voltage-dependent Ca2+ channels; VSMC, vascular smooth muscle cells
论文方向：[{"id":13,"name":"细胞生物学"},{"id":879,"name":"生物化学"}]
发表期刊：FEBS Letters Volume 554, Issue 3
发表时间：Thu Nov 20 00:00:00 CST 2003
数字识别码：10.1016/S0014-5793(03)01198-0
是否作者本人： 否
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