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Enhanced Levels of microRNA-125b in Vascular Smooth Muscle Cells of Diabetic db/db Mice Lead to Increased Inflammatory Gene Expression by Targeting the Histone Methyltransferase Suv39h1

机译:通过靶向组蛋白甲基转移酶Suv39h1,增强糖尿病db / db小鼠血管平滑肌细胞中microRNA-125b的水平,导致炎症基因表达增加。

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摘要

Diabetes remains a major risk factor for vascular complications that seem to persist even after achieving glycemic control, possibly due to "metabolic memory." Using cultured vascular smooth muscle cells (MVSMC) from type 2 diabetic db/db mice, we recently showed that decreased promoter occupancy of the chromatin histone H3 lysine-9 methyltransferase Suv39h1 and the associated repressive epigenetic mark histone H3 lysine-9 trimethylation (H3K9me3) play key roles in sustained inflammatory gene expression. Here we examined the role of microRNAs (miRs) in Suv39h1 regulation and function in MVSMC from diabetic mice.
机译:糖尿病仍然是血管并发症的主要危险因素,即使达到血糖控制后,血管并发症似乎仍然存在,这可能是由于“代谢记忆”造成的。使用来自2型糖尿病db / db小鼠的培养的血管平滑肌细胞(MVSMC),我们最近发现染色质组蛋白H3赖氨酸9甲基转移酶Suv39h1和相关的抑制性表观遗传标记组蛋白H3赖氨酸9三甲基化(H3K9me3)的启动子占用降低在持续的炎症基因表达中起关键作用。在这里,我们检查了糖尿病小鼠MVSMC中microRNA(miRs)在Suv39h1调节和功能中的作用。

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  • 来源
    《Diabetes》 |2010年第11期|p.2904-2915|共12页
  • 作者单位

    From the Department of Diabetes, Beckman Research Institute of City of Hope, Duarte, California.Corresponding author: Rama Natarajan, RNatarajan@coh.org.Received 10 February 2010 and accepted 13 July 2010. Published ahead of print at http://diabetes.diabetesiiounials.org on 10 August 2010, DOL 10.2337^10-0208.© 2010 by the American Diabetes Association, Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommon5.org/liceiises/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in pan by tiie payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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