کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6155850 | 1597938 | 2016 | 38 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deletion of sirtuin 6 accelerates endothelial dysfunction and atherosclerosis in apolipoprotein E-deficient mice
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کلمات کلیدی
mRNAmouse aortic endothelial cellsMAECssirtuin 6SIRT6OROVCAM-1MCP-1HUVECHCDICAM-1NF-κBHDLshRNAGAPDHApoE−/− - ApoE - / -high-density lipoprotein - HDL یا لیپوپروتئین با دانسیته بالا یا چگالی بالاmessenger RNA - RNA messengerSmall interfering RNA - RNA تداخل کوچکsmall hairpin RNA - RNA کوچک موی سرsiRNA - siRNAOil red O - روغن قرمز OHigh-cholesterol diet - رژیم غذایی با کلسترول بالاHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانnuclear factor-κB - فاکتور هسته ای κBLow-density lipoprotein - لیپوپروتئین کم چگالی یا الدیال LDL - لیپوپروتئین کم چگالی(کلسترول بد)intracellular adhesion molecule-1 - مولکول چسبندگی داخل سلولی -1vascular cellular adhesion molecule-1 - مولکول چسبندگی سلولی عروقی-1monocyte chemotactic protein 1 - پروتئین chemotactic monocyte 1glyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
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چکیده انگلیسی
Sirtuin 6 (SIRT6) is a chromatin-associated deacetylase that plays a leading role in genomic stability and aging. However, the precise role of SIRT6 in atherosclerosis, an aging-associated cardiovascular disease, remains elusive. This study aims at defining the role of SIRT6 in atherosclerotic lesion development. SIRT6 messenger RNA and protein expression are markedly decreased in atherosclerotic aortas of apolipoprotein E-deficient (ApoEâ/â) mice fed a high-cholesterol diet. SIRT6 was knocked down in ApoEâ/â mice using small hairpin RNAs (shRNAs) lentivirus injection. SIRT6-shRNA-treated ApoEâ/â mice showed impaired endothelium-dependent vasodilation, increased plaque size (in aortic sinus, aortic root and en face aorta), and augmented plaque vulnerability (evidenced by increased necrotic core areas and macrophage accumulation and reduced collagen content). At the cellular level, SIRT6 depletion by RNA interference in human umbilical vein endothelial cells significantly increased monocyte adhesion to endothelial cells by inducing the expression of intracellular adhesion molecule-1. Consistently, intracellular adhesion molecule-1 expression was significantly upregulated in aortic endothelium of SIRT6-shRNA-treated ApoEâ/â mice compared with controls. In sum, the aforementioned findings suggest that SIRT6 is a primary negative regulation factor in endothelial dysfunction and atherosclerosis development. As a result, SIRT6 is a promising therapeutic target for treating atherosclerosis and its cardiovascular complications.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 172, June 2016, Pages 18-29.e2
Journal: Translational Research - Volume 172, June 2016, Pages 18-29.e2
نویسندگان
Zhiping Liu, Jiaojiao Wang, Xiaoyang Huang, Zhuoming Li, Peiqing Liu,