کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1910304 | 1046763 | 2009 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hypothermic preconditioning of endothelial cells attenuates cold-induced injury by a ferritin-dependent process
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
HO-1HBSSBDIGSSGHeme oxygenase-1EGMEBMHCAEC12-O-tetradecanoylphorbol 13-acetateGSHtPADFOhypothermic preconditioningHPCIRE-BPDeferoxamine3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide - 3- [4،5-dimethylthiazol-2-yl] -2،5-difenyl tetrazolium bromideMTT - MTTUniversity of Wisconsin - دانشگاه ویسکانسینFree radicals - رادیکال آزادHuman coronary artery endothelial cell - سلول اندوتلیال عروق کرونر انسانیEndothelial cells - سلولهای اندوتلیالFerritin - فریتینlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Hanks' balanced salt solution - محلول نمک متعادل هانکسendothelial basal medium - محیط بازال اندوتلیالendothelial growth medium - محیط رشد اندوتلیالheme oxygenase - همگام اکسژنازHypothermia - هیپوترمیPreconditioning - پیش شرط بندیreduced glutathione - کاهش گلوتاتیونoxidized glutathione - گلوتاتیون اکسید شدهtotal glutathione - گلوتاتیون کل
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Hypothermia for myocardial protection or storage of vascular grafts may damage the endothelium and impair vascular function upon reperfusion/rewarming. Catalytic iron pools and oxidative stress are important mediators of cold-induced endothelial injury. Because endothelial cells are highly adaptive, we hypothesized that hypothermic preconditioning (HPC) protects cells at 0°C by a heme oxygenase-1 (HO-1) and ferritin-dependent mechanism. Storage of human coronary artery endothelial cells at 0°C caused the release of lactate dehydrogenase, increases in bleomycin-detectible iron (BDI), and increases in the ratio of oxidized/reduced glutathione, signifying oxidative stress. Hypoxia increased injury at 0°C but did not increase BDI or oxidative stress further. HPC at 25°C for 15-72 h attenuated these changes by an amount achievable by pretreating cells with 10-20 μM deferoxamine, an iron chelator, and protected cell viability. Treating cells with hemin chloride at 37°C transiently increased intracellular heme, HO-1, BDI, and ferritin. Elevated heme/iron sensitized cells to 0°C but ferritin was protective. HPC increased iron maximally after 2 h at 25°C and ferritin levels peaked after 15 h. HO-1 was not induced. When HPC-mediated increases in ferritin were blocked by deferoxamine, protection at 0°C was diminished. We conclude that HPC-mediated endothelial protection from hypothermic injury is an iron- and ferritin-dependent process.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 46, Issue 5, 1 March 2009, Pages 680-691
Journal: Free Radical Biology and Medicine - Volume 46, Issue 5, 1 March 2009, Pages 680-691
نویسندگان
Michael A.J. Zieger, Mahesh P. Gupta,