کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1910190 | 1046757 | 2009 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cigarette smoke extract induces cytosolic phospholipase A2 expression via NADPH oxidase, MAPKs, AP-1, and NF-κB in human tracheal smooth muscle cells
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کلمات کلیدی
BCAbicinchoninic acid protein assayDMEM/F-12p47phoxc-Jun NH2-terminal kinaseDCF-DAcPLA2AP-1DPIGAPDHNACCSENF-κBPBSCOXFBSJnkMAPK - MAPKMAPKs - MAPK هاN-acetylcysteine - N-استیل سیستئینROS - ROSsiRNA - siRNAcyclooxygenase - آنزیم سیکلواکسیژنازapo - آپوApocynin - آپوسیینینArachidonic acid - اسید آراشیدونیکNADPH oxidase - اکسیداز NADPH COPD - بیماری مزمن انسدادی ریهChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهdiphenyleneiodonium chloride - دی فینیلنیدونیم کلریدfetal bovine serum - سرم جنین گاوcigarette smoke extract - عصاره سیگار سیگارnuclear factor-κB - فاکتور هسته ای κBcytosolic phospholipase A2 - فسفولیپاز A2 سیتوزولPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریactivator protein-1 - پروتئین فعال کننده-1mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenprostaglandin - پروستاگلاندینهاglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Up-regulation of cytosolic phospholipase A2 (cPLA2) by cigarette smoke extract (CSE) may play a critical role in airway inflammatory diseases. However, the mechanisms underlying CSE-induced cPLA2 expression in human tracheal smooth muscle cells (HTSMCs) remain unknown. CSE induced cPLA2 protein and mRNA expression, and ROS generation was attenuated by pretreatment with a reactive oxygen species (ROS) scavenger (N-acetylcysteine), or inhibitors of NADPH oxidase (diphenyleneiodonium chloride, apocynin) and transfection with p47phox siRNA, suggesting that CSE-induced cPLA2 expression was mediated through NADPH oxidase activation and ROS production in HTSMCs. Furthermore, CSE-induced cPLA2 expression was attenuated by pretreatment with the inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), and JNK (SP600125), which were further confirmed by transfection with siRNAs of JNK1, p42, and p38 to down-regulate the expression of respective proteins and reduce cPLA2 expression. Induction of cPLA2 by CSE was attenuated by selective inhibitors of NF-κB (helenalin) and AP-1 (curcumin). Moreover, promoter assays revealed that increases of cPLA2, NF-κB, and AP-1 luciferase activities stimulated by CSE were attenuated by these inhibitors. These results suggest that in HTSMCs, CSE induced NADPH oxidase activation leading to phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK. These reactions induced nuclear transcription NF-κB and AP-1 activities which were essential for CSE-induced cPLA2 gene expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 46, Issue 7, 1 April 2009, Pages 948-960
Journal: Free Radical Biology and Medicine - Volume 46, Issue 7, 1 April 2009, Pages 948-960
نویسندگان
Shin-Ei Cheng, Shue-Fen Luo, Mei-Jie Jou, Chih-Chung Lin, Yu Ru Kou, I-Ta Lee, Hsi-Lung Hsieh, Chuen-Mao Yang,