Induced proliferation of human MRC-5 cells by nitrogen oxides via direct and indirect activation of MEKK1, JNK, and p38 signals.

doi:10.1006/taap.2002.9415

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/10823

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Title:	Induced proliferation of human MRC-5 cells by nitrogen oxides via direct and indirect activation of MEKK1, JNK, and p38 signals.
Authors:	Chou, FP Tseng, TH Chen, JH Wang, HC Wang, CJ
Contributors:	中山醫學大學
Keywords:	nitrogen oxides;human lung fibroblast cells (MRC-5);proliferation;NF-κB;iNOS;MEKK1;JNK, and p38
Date:	2002
Issue Date:	2015-05-15T05:40:06Z (UTC)
ISSN:	0041-008X
Abstract:	Nitrogen oxides (NOx) are important indoor air pollutants and an occupational hazard. Many studies demonstrated that NOx causes lung tissue damage based on the oxidation properties and the free-radical potentials of these gases. In this study we found that NOx delivered as a NO gas-saturated solution induced proliferation of human lung fibroblast MCR-5 cells as evidenced by increasing cell number and S phase distribution. Western data showed that NOx increased the expressions of c-Fos, c-Jun, and signaling kinases including MEKK1, JNK1, and p38 (with induction fold of 3.3, 2.8, and 3.2, respectively) in the cells 12 h after treatment. The levels of phospho-MEKK1 and phospho-JNK1 were also increased. The application of iNOS inhibitor, NAME, partially blocked the activation of MEKK4 and JNK1. These data suggested that JNK and p38 signaling kinases are activated partly by endogenous NO that are generated from NOx-activated iNOS in MRC-5 cells. Therefore, the NOx-induced cell proliferation via activation of MEKK1, JNK1, and p38 might contribute to lung tissue damage caused by NOx pollutants. (c) 2002 Elsevier Science (USA).
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10823 http://dx.doi.org/10.1006/taap.2002.9415
Relation:	Toxicol Appl Pharmacol. 2002 Jun 15;181(3):203-8.
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

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