کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10954328 | 1097897 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TGF-β1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation
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کلمات کلیدی
PKCTGF-βMAPKKKTAK1ANFBNPET-1ATFAngiotensin II - آنژیوتانسین دوendothelin-1 - اندوتلین-1transforming growth factor-β - تبدیل فاکتور رشد βAng II - دومCytokine - سیتوکینdominant negative - غالب منفی استatrial natriuretic factor - فاکتور natriuretic دهلیزیProtein phosphorylation - فسفوریلاسیون پروتئینactivating transcription factor - فعال کردن عامل رونویسیmyocyte - میوسیتHypertrophy - هیپرتروفی یا پُرسازیProtein kinase C - پروتئین کیناز سیmitogen-activated protein kinase kinase kinase - پروتئین کیناز کیناز کیناز پروتئین فعال Mitogenbrain natriuretic peptide - پپتید ناتریورتیک مغزیMAP kinase - کیناز MAP
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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![عکس صفحه اول مقاله: TGF-β1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation TGF-β1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation](/preview/png/10954328.png)
چکیده انگلیسی
Several reports have suggested that the TAK1-MKK3/6-p38MAPK signaling axis is important for TGF-β-related cardiac hypertrophy. Despite this, the effects of exogenous TGF-β on cardiac hypertrophy and associated signaling mechanisms have not been demonstrated directly. Moreover, the roles of the signaling mechanisms involved in cardiac hypertrophy (TAK1 upstream and p38MAPK downstream) remain unclear. In this study, we investigated the potential involvement of protein kinase C and activating transcription factor-2 in TGF-β1-induced cardiac hypertrophic responses in cultured neonatal rat ventricular cardiomyocytes. TGF-β1 treatment resulted in upregulation of mRNA expression or promoter activities of β-myosin heavy chain, atrial natriuretic factor, and brain natriuretic peptide, and increased myocyte protein content, cell size, and sarcomeric organization. These are all characteristic hallmarks of cardiac hypertrophy. PKC was found to be involved throughout the signaling system, and it was shown that it acts by mediating upstream TAK1 activation and leads to ATF-2 activation. PKC-dependent ATF-2 activation was shown to be involved in TGF-β1-induced cardiac hypertrophic responses. The PKC inhibitors, GO6976 and GF109203X, completely blocked TGF-β1-induced TAK1 kinase activity and subsequent downstream signaling pathways including ATF-2 phosphorylation, leading to suppression of ATF-2 transcriptional activity. This inhibitory effect was reflected in cardiac hypertrophic responses such as inhibitions of β-MHC gene induction and ANF promoter activity. Our results suggest that PKC is involved in TGF-β1-induced cardiac hypertrophic responses in our cell culture system and that ATF-2 activation plays a role.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 4, October 2005, Pages 627-636
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 4, October 2005, Pages 627-636
نویسندگان
Joong-Yeon Lim, Sung Joon Park, Ha-Young Hwang, Eun Jung Park, Jae Hwan Nam, Joon Kim, Sang Ick Park,