کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739351 | 1046872 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lung epithelial cells release ATP during ozone exposure: Signaling for cell survival
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کلمات کلیدی
2-DeoxyglucoseTECsVesicularCytochalasin BHBSSERKFAKSAGMELF2-DOGFBSSDSDMEMDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccoadenosine deaminase - آدنوزین دآمینازATP release - آزادی ATPAkt - آکتOzone - اُزون Cell survival - بقای سلولیBAPTA-AM - بیایپیتیای-AMGlucose uptake - جذب گلوکزApoptosis - خزان یاختهایTER - داشتنsodium dodecyl sulfate - سدیم دودسیل سولفاتfetal bovine serum - سرم جنین گاوSmall airway epithelial cells - سلول های اپیتلیال کوچک هواپیماHuman lung microvascular endothelial cells - سلولهای اندوتلیوم میکروویو انسانی ریه انسانTracheal epithelial cells - سلولهای اپیتلیال تراشهLung epithelial cells - سلولهای اپیتلیال ریهEpithelial lining fluid - مایع تخلیه اپیتلیالMEK - مجاهدین خلقHank's balanced salt solution - محلول نمک متعادل هانکTransepithelial resistance - مقاومت TransepithelialADA - وجود داردfocal adhesion kinase - کیناز چسبندگی کانونی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
The common air pollutant ozone causes acute toxicity to human airways. In primary and transformed epithelial cells from all levels of human or rat airways, ozone levels relevant to air pollution (50-200 ppb) increased extracellular [ATP] within 7-30 min. A human bronchial epithelial cell line (16HBE14o-) that forms electrically resistant polarized monolayers had up to 10-fold greater apical than basolateral surface extracellular [ATP] within 7 min of ozone exposure. Increased extracellular [ATP] appeared due to ATP secretion or release because (1) inhibition of ectonucleotidase (cell surface enzyme(s) which degrade ATP) by ozone did not occur until >120 min of ozone exposure and (2) brefeldin A, a secretory inhibitor, eliminated elevation of extracellular [ATP] without affecting intracellular ATP. Extracellular ATP protected against ozone toxicity in a P2Y receptor-dependent manner as (1) removal of ATP and adenosine by apyrase and adenosine deaminase, respectively, potentiated ozone toxicity, (2) extracellular supplementation with ATP, a poorly hydrolyzable ATP analog ATPγS, or UTP inhibited apoptotic and necrotic ozone-mediated cell death, and (3) ATP-mediated protection was eliminated by P2 and P2Y receptor inhibitors suramin and Cibacron blue (reactive blue 2), respectively. The decline in glucose uptake caused by prolonged ozone exposure was prevented by supplemental extracellular ATP, an effect blocked by suramin. Further, Akt and ERK phosphorylation resulted from exposure to supplemental extracellular ATP. Thus, extracellularly released ATP signals to prevent ozone-induced death and supplementation with ATP or its analogs can augment protection, at least in part via Akt and /or ERK signaling pathways and their metabolic effects.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 2, 15 July 2005, Pages 213-226
Journal: Free Radical Biology and Medicine - Volume 39, Issue 2, 15 July 2005, Pages 213-226
نویسندگان
Shama Ahmad, Aftab Ahmad, Glen McConville, Barbara K. Schneider, Corrie B. Allen, Rizwan Manzer, Robert J. Mason, Carl W. White,