Induction of apoptosis in the lung tissue from rats exposed to cigarette smoke involves p38/JNK MAPK pathway.

doi:10.1016/j.cbi.2005.04.008

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 310902500/10800

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10800

Title:	Induction of apoptosis in the lung tissue from rats exposed to cigarette smoke involves p38/JNK MAPK pathway.
Authors:	Kuo, WH Chen, JH Lin, HH Chen, BC Hsu, JD Wang, CJ
Contributors:	中山醫學大學
Keywords:	Apoptosis;Cigarette smoke;Lung pathogenesis;MAP kinase;Caspase cascade
Date:	2005
Issue Date:	2015-05-11T10:29:23Z (UTC)
ISSN:	0009-2797
Abstract:	Smoking is a major cause of human lung cancer. Past studies suggest that apoptosis might influence the malignant phenotype, but little is known about the association between apoptosis and cigarette smoke (CS)-induced lung pathogenesis. Using an in situ cell death detection kit (TA300), the association of CS with apoptosis was determined in a concentration-dependent manner. Furthermore, the expression of related proteins were investigated in the terminal bronchiole areas of the lung tissue from rats exposed to CS. Results showed that the expression of phosphotyrosine proteins was increased significantly in lung tissue of rats exposed to CS from 5 to 15 cigarettes. Using Western blotting and immunoprecipitation assay, Fas, a death receptor, was proved just be one of these phosphotyrosine proteins. CS triggered activation of MAP kinase (p38/JNK or ERK2) pathway, which led to Jun or p53 phosphorylation and FasL induction links Fas phosphorylation. Further, smoke treatment produced an increase in the level of proapoptotic proteins (Bax, t-Bid, cytochrome c and caspase-3), but a decline in Bcl-2, procaspase-8 and procaspase-9 proteins. Thus, CS-induced apoptosis may result from two main mechanisms, one is the activation of p38/JNK-Jun-FasL signaling, and the other is stimulated by the stabilization of p53, increase in the ratio of Bax/Bcl-2, release of cytochrome c; thus, leading to activation of caspase cascade.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10800 http://dx.doi.org/10.1016/j.cbi.2005.04.008
Relation:	Chem Biol Interact. 2005 Jun 30;155(1-2):31-42.
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

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