کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9029471 | 1561661 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Induction of apoptosis in the lung tissue from rats exposed to cigarette smoke involves p38/JNK MAPK pathway
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کلمات کلیدی
ERK2protein kinase C-αPKC-αB cell lymphoma-2MEK1Bcl-2Jnkc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKSDS–PAGE - SDS-PAGEStat1 - sTAT1Caspase cascade - آبشار کاسپازsodium dodecyl sulphate–polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدBax - باکسtruncated Bid - تضعیف مزایدهApoptosis - خزان یاختهایCigarette smoke - دود سیگارFas Ligand - فاس لیگاندFasL - فاسدBcl-2 Associated X protein - پروتئین Bcl-2 Associated XMAP kinase - کیناز MAP
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 155, Issues 1â2, 30 June 2005, Pages 31-42
Journal: Chemico-Biological Interactions - Volume 155, Issues 1â2, 30 June 2005, Pages 31-42
نویسندگان
Wu-Hsien Kuo, Jing-Hsien Chen, Hui-Hsuan Lin, Bi-Chiou Chen, Jeng-Dong Hsu, Chau-Jong Wang,