کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8322454 | 1539875 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of MEF2A prevents hyperglycemia-induced extracellular matrix accumulation by blocking Akt and TGF-β1/Smad activation in cardiac fibroblasts
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کلمات کلیدی
STZJun NH2-terminal kinaseshRNAsLVPW7-amino-actinomycin D7-AADTIMP1MEF2ALVESDLVEDdIVSECMCCK-8MMPTGF-β1CFSJnkE/A - E / AERK1/2 - ERK1 / 2MAPK - MAPKMOI - MERNA interference - RNA تداخل کنندهRNAi - RNA سرکوبگر،RNA مداخلهگر، RNA خاموش کنندهLeft ventricular end-diastolic dimension - ابعاد انتهایی دیاستولیک بطن چپstreptozotocin - استرپتوزوتوسینCardiac remodeling - بازسازی قلبDiabetes - بیماری قندTransforming growth factor-β1 - تبدیل فاکتور رشد β1cell counting kit-8 - شمارش سلول کیت 8phycoerythrin - فایکوئیریدینcardiac fibroblasts - فیبروبلاست های قلبExtracellular matrix - ماتریکس خارج سلولیmatrix metalloproteinase - ماتریکس متالوپروتئینازTissue inhibitor of metalloproteinase - مهار کننده های متالوپروتئیناز بافتHyperglycemic - هیپرگلیسمیmultiplicity of infection - چندین عفونتejection fraction - کسری خروجیfractional shortening - کوتاه کردن کسریmitogen-activated protein kinases - کیناز پروتئین فعال Mitogenhigh glucose - گلوکز بالا یا قند بالاnormal glucose - گلوکز طبیعی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Myocyte enhancer factor 2A (MEF2A) functions in muscle-specific and/or growth factor-related transcription and is involved in cell growth, survival, and apoptosis. To evaluate the role of this transcription factor in cardiac fibroblasts (CFs) in diabetes mellitus, we performed a series of in vitro and in vivo experiments. We used short hairpin RNA (shRNA) to inhibit the expression of MEF2A in CFs in vitro. Inhibition of MEF2A significantly reduced hyperglycemia-induced CF proliferation and migration, myofibroblast differentiation, matrix metalloproteinase (MMP) activities, and collagen production. Furthermore, MEF2A inhibition attenuated HG-induced activation of the mitogen-activated protein kinase (MAPK), Akt, and TGF-β1/Smad signaling pathways. For in vivo analysis in a mouse model, type-1 diabetes was induced by streptozotocinand MEF2A expression was knocked down by myocardial injection with lentivirus carrying shRNA-MEF2A. Cardiac function was assessed by echocardiography. Total collagen deposition was assessed by Masson's trichrome and Picrosirius red staining. Knockdown of MEF2A ameliorated diabetes-induced cardiac dysfunction and collagen deposition. Our study suggests that inhibition of MEF2A could alleviate HG-induced extracellular matrix accumulation by blocking the activation of Akt and TGF-β1/Smad signaling pathway in CFs. Thus, inhibition of MEF2A has therapeutic potential in the treatment of diabetic-induced cardiac remodeling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 69, December 2015, Pages 52-61
Journal: The International Journal of Biochemistry & Cell Biology - Volume 69, December 2015, Pages 52-61
نویسندگان
Xueying Chen, Guoliang Liu, Wei Zhang, Jianing Zhang, Yugang Yan, Wenqian Dong, Ershun Liang, Yun Zhang, Mingxiang Zhang,