期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 225, 期 3, 页码 741-750出版社
WILEY
DOI: 10.1002/jcp.22270
关键词
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资金
- National Science Council, Taiwan [NSC97-2321-B-182-007, NSC98-2321-B-182-004, NSC96-2320-B-182-009]
- Chang Gung Medical Research Foundation, Taiwan [CMRPD150253, CMRPD150313, CMRPD170492, CMRPD180371]
Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-I expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30 mu g/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS. J. Cell, Physiol. 225: 741-750, 2010. (C) 2010 Wiley-Liss, Inc.
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