کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738006 | 1046678 | 2011 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
β1-Integrin is up-regulated via Rac1-dependent reactive oxygen species as part of the hypertrophic cardiomyocyte response
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کلمات کلیدی
DMEMDcfANPFAKERKEGFRET-15-bromo-2-deoxyuridineβ-MHCDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccoendothelin-1 - اندوتلین-1BrdU - بروموداکسی اوریدینdichlorofluorescein diacetate - دی کللت فلوئورسین دی سکتهβ-myosin heavy chain - زنجیره سنگین بتا-میوزینatrial natriuretic peptide - پپتید نایروئیدوری دهلیزextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیfocal adhesion kinase - کیناز چسبندگی کانونیadrenergic receptor - گیرنده آدرنرژیکEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
β1-Integrin mediates cardiomyocyte growth and survival and its proper regulation is essential for the structural and functional integrity of the heart. β1-Integrin expression is enhanced in hypertrophy, but the mechanism and significance of its up-regulation are unknown. Because reactive oxygen species (ROS) are important mediators of myocardial remodeling we examined their role in regulated β1-integrin expression. Hypertrophy was induced in neonatal cardiomyocytes by endothelin-1 (ET-1), which activated the regulatory NADPH oxidase subunit Rac1, evoked ROS, and enhanced fetal gene expression and cardiomyocyte size. ET-1 also enhanced cell adhesion and FAK phosphorylation and inhibited oxidative stress-induced cardiomyocyte apoptosis. Further, ET-1 increased β1-integrin mRNA and protein expression via Rac1-ROS-dependent MEK/ERK and EGF receptor-PI3K/Akt activation as shown by adenoviral dominant-negative Rac1 or overexpression of copper/zinc-superoxide dismutase. The relevance of regulated β1-integrin expression was examined in cardiomyocytes, in which targeting siRNA impeded the ET-1-induced β1-integrin up-regulation. In these cells, ET-1-induced cell adhesion, FAK phosphorylation, and hypertrophic response were significantly blunted, whereas its antiapoptotic effect was predominantly unchanged, suggesting at least partial dissociation of prohypertrophic and prosurvival signaling elicited by ET-1. In conclusion, β1-integrin up-regulation in response to ET-1 is mediated via Rac1-ROS-dependent activation of prohypertrophic pathways and is mandatory for ET-1-induced FAK activation, cell adhesion, and hypertrophic response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 3, 1 August 2011, Pages 609-618
Journal: Free Radical Biology and Medicine - Volume 51, Issue 3, 1 August 2011, Pages 609-618
نویسندگان
Stéphanie P. Häuselmann, Berit I. Rosc-Schlüter, Vera Lorenz, Isabelle Plaisance, Marijke Brink, Otmar Pfister, Gabriela M. Kuster,