کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10758298 | 1050406 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-214 provokes cardiac hypertrophy via repression of EZH2
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Micro RNAs are small, non-coding RNA molecules that regulate gene expression via either translational inhibition or mRNA degredation. Enhancer of zeste homolog 2 (EZH2)-mediated hypertrophic signaling is a major regulatory response to hypertrophic stimuli. In this study, we constructed AAC rat models and PE-induced hypertrophic cardiomyocytes. We demonstrated that miR-214 relative levels were upregulated, whereas EZH2 was downregulated in both vivo and vitro models. Further, one conserved base-pairing site in the EZH2 3â²-untranslated region (UTR) was verified. Mutation of the site in the EZH2 3â²-UTR completely blocked the negative effect of miR-214 on EZH2, suggesting that EZH2 is a direct target for miR-214 regulation. Using a gain-of-function approach, incorporating the lentivirus constructed miR-214 and its sponge, we demonstrated that miR-214 significantly regulated endogenous levels of EZH2 gene expression; whereas, changes in the expression of the Sine oculis homeobox homolog gene were induced by an adrenergic receptor agonist in the AAC rat model. Having made this study it is possible to conclude that the negative regulation of EZH2 expression contributed to miR-214-mediated cardiac hypertrophy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 436, Issue 4, 12 July 2013, Pages 578-584
Journal: Biochemical and Biophysical Research Communications - Volume 436, Issue 4, 12 July 2013, Pages 578-584
نویسندگان
Tao Yang, Guo-fei Zhang, Xiao-fan Chen, Hai-hua Gu, Shao-zi Fu, Hong-feng Xu, Qiang Feng, Yi-Ming Ni,