کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5905857 | 1159942 | 2017 | 29 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cardiac-specific Traf2 overexpression enhances cardiac hypertrophy through activating AKT/GSK3β signaling
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کلمات کلیدی
ANPGAPDHTACBNPβ-MHCGSK3βTRAF2LVEDdLVESDAkt - آکتPressure overload - بیش از حد فشارβ-myosin heavy chain - زنجیره سنگین بتا-میوزینtumor necrosis factor receptor-associated factor 2 - عامل گیرنده فاکتور نکروز تومور عامل 2Cardiomyocyte - قلب و عروقpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازatrial natriuretic peptide - پپتید نایروئیدوری دهلیزB-type natriuretic peptide - پپتید نیترویوتیک B نوعglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Tumor necrosis factor superfamily ligands provoke a dilated cardiac phenotype signal through a common scaffolding protein termed tumor necrosis factor receptor-associated factor 2 (Traf2); however, Traf2 signaling in the adult mammalian cardiac hypertrophy is not fully understood. This study was aimed to identify the effect of Traf2 on cardiac hypertrophy and the underlying mechanisms. A significant up-regulation of Traf2 expression was observed in mice failing hearts. To further investigate the role of Traf2 in cardiac hypertrophy, we used cultured neonatal rat cardiomyocytes with gain and loss of Traf2 function and cardiac-specific Traf2-overexpressing transgenic (TG) mice. In cultured cardiomyocytes, Traf2 positively regulated angiotensin II (Ang II)-mediated hypertrophic growth, as detected by [3H]-Leucine incorporation, cardiac myocyte area, and hypertrophic marker protein levels. Cardiac hypertrophy in vivo was produced by constriction of transverse aortic (TAC) in TG mice and their wild-type controls. The extent of cardiac hypertrophy was evaluated by echocardiography as well as by pathological and molecular analyses of heart samples. Traf2 overexpression in the heart remarkably enhanced cardiac hypertrophy, left ventricular dysfunction in mice in response to TAC. Further analysis of the signaling pathway in vitro and in vivo suggested that these adverse effects of Traf2 were associated with the activation of AKT/glycogen synthase kinase 3β (GSK3β). The present study demonstrates that Traf2 serves as a novel mediator that enhanced cardiac hypertrophy by activating AKT/GSK3β signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Brought to you by:College of Engineering Chengannur - 'Renewal due by 31 Dec 2017'
Journal: Gene - Brought to you by:College of Engineering Chengannur - 'Renewal due by 31 Dec 2017'
نویسندگان
Yinqing Huang, Dengyin Wu, Xin Zhang, Minghua Jiang, Chaohui Hu, Jiangfeng Lin, Jifei Tang, Lianpin Wu,