کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10802102 | 1055658 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lysine methyltransferase Smyd2 suppresses p53-dependent cardiomyocyte apoptosis
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کلمات کلیدی
CoCl2terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labelingSMYD2PARP17-AAGHSP90PNAp53Myocardial infarction - آنفارکتوس میوکاردTUNEL - تونلApoptosis - خزان یاختهایRetinoblastoma tumor suppressor - سرکوب کننده تومور رتینوبلاستوماCardiomyocyte - قلب و عروقLAD - لادوheart failure - نارسایی قلبیHeat shock protein 90 - پروتئین شوک حرارت 90poly ADP ribose polymerase - پلی ADA ریبوز پلی مرازleft anterior descending artery - چپ قوام نزولی شریانCobalt chloride - کلرید کبالت
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Apoptosis, or programmed cell death, is an essential physiological process for proper embryogenesis as well as for homeostasis during aging. In addition, apoptosis is one of the major mechanisms causing cell loss in pathophysiological conditions such as heart failure. Thus, inhibition of apoptosis is an important approach for preventive and therapeutic strategies. Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis. Smyd2 protein levels were significantly decreased in cardiomyocytes upon cobalt chloride-induced apoptosis or myocardial infarction, while p53 expression was enhanced. siRNA-mediated knockdown of Smyd2 in cultured cardiomyocytes further enhanced cobalt chloride-induced cardiomyocyte apoptosis. In contrast, Smyd2 overexpression resulted in marked methylation of p53 and prevented its accumulation as well as apoptotic cell death in an Hsp90-independent manner. Moreover, overexpression, of Smyd2, but not Smyd2Y240F lacking a methyl transferase activity, significantly rescued CoCl2-induced apoptosis in H9c2 cardioblasts. Finally, Smyd2 cardiomyocyte-specific deletion in vivo promoted apoptotic cell death upon myocardial infarction, which correlated with enhanced expression of p53 and pro-apoptotic Bax. Collectively, our data indicate Smyd2 as a cardioprotective protein by methylating p53.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1843, Issue 11, November 2014, Pages 2556-2562
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1843, Issue 11, November 2014, Pages 2556-2562
نویسندگان
Amna Sajjad, Tatyana Novoyatleva, Silvia Vergarajauregui, Christian Troidl, Ralph T. Schermuly, Haley O. Tucker, Felix B. Engel,