کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8269937 | 1534966 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nicotine mediates oxidative stress and apoptosis through cross talk between NOX1 and Bcl-2 in lung epithelial cells
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کلمات کلیدی
Bcl-2BIS IAlveolar epithelial type II cellsNOX1BEAS-2BAECα-Bgtα-bungarotoxinnAChRPBSDMSO - DMSONOx - NOXROS - ROSNADPH oxidase - اکسیداز NADPH bisindolylmaleimide I - بیستینولیل مولارین IOxidative stress - تنش اکسیداتیوApoptosis - خزان یاختهایdihydroethidium - دی هیدروتیدیمDimethyl sulfoxide - دیمتیل سولفواکسیدFree radicals - رادیکال آزادalveolar epithelial cell - سلول های اپیتلیال آلوئولارendoplasmic reticulum - شبکه آندوپلاسمی Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریwild type - نوع وحشیNicotine - نیکوتین DHE - وWestern blot - وسترن بلاتReactive oxygen species - گونههای فعال اکسیژنnicotinic acetylcholine receptor - گیرنده استیلکولین نیکوتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Nicotine contributes to the onset and progression of several pulmonary diseases. Among the various pathophysiological mechanisms triggered by nicotine, oxidative stress and cell death are reported in several cell types. We found that chronic exposure to nicotine (48Â h) induced NOX1-dependent oxidative stress and apoptosis in primary pulmonary cells. In murine (MLE-12) and human (BEAS-2B) lung epithelial cell lines, nicotine acted as a sensitizer to cell death and synergistically enhanced apoptosis when cells were concomitantly exposed to hyperoxia. The precise signaling pathway was investigated in MLE-12 cells in which NOX1 was abrogated by a specific inhibitor or stably silenced by shRNA. In the early phase of exposure (1Â h), nicotine mediated intracellular Ca2+ fluxes and activation of protein kinase C, which in its turn activated NOX1, leading to cellular and mitochondrial oxidative stress. The latter triggered the intrinsic apoptotic machinery by modulating the expression of Bcl-2 and Bax. Overexpression of Bcl-2 completely prevented nicotine's detrimental effects, suggesting Bcl-2Â as a downstream key regulator in nicotine/NOX1-induced cell damage. These results suggest that NOX1 is a major contributor to the generation of intracellular oxidative stress induced by nicotine and might be an important molecule to target in nicotine-related lung pathologies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 76, November 2014, Pages 173-184
Journal: Free Radical Biology and Medicine - Volume 76, November 2014, Pages 173-184
نویسندگان
Filippo Zanetti, Marta Giacomello, Yves Donati, Stephanie Carnesecchi, Maud Frieden, Constance Barazzone-Argiroffo,