کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10750721 | 1050302 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigenetic priming of inflammatory response genes by high glucose in adipose progenitor cells
ترجمه فارسی عنوان
پر ژیپی اپی ژنتیک ژن پاسخ التهابی با استفاده از گلوکز بالا در سلول های پیش ساز چربی
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کلمات کلیدی
TSSASCMSCHistone modification - اصلاح هیستونinflammation - التهاب( توروم) chromatin immunoprecipitation - ایمن سازی کروماتینGene expression - بیان ژنtranscription start site - رونویسی شروع سایتMesenchymal stromal cell - سلول استروما MesenchymalAdipose stem cell - سلول بنیادی چربیGene ontology - هستیشناسی ژنیInflammation response - پاسخ التهابCHiP - چیپChromatin - کروماتینGlucose - گلوکز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Cellular metabolism confers wide-spread epigenetic modifications required for regulation of transcriptional networks that determine cellular states. Mesenchymal stromal cells are responsive to metabolic cues including circulating glucose levels and modulate inflammatory responses. We show here that long term exposure of undifferentiated human adipose tissue stromal cells (ASCs) to high glucose upregulates a subset of inflammation response (IR) genes and alters their promoter histone methylation patterns in a manner consistent with transcriptional de-repression. Modeling of chromatin states from combinations of histone modifications in nearly 500 IR genes unveil three overarching chromatin configurations reflecting repressive, active, and potentially active states in promoter and enhancer elements. Accordingly, we show that adipogenic differentiation in high glucose predominantly upregulates IR genes. Our results indicate that elevated extracellular glucose levels sensitize in ASCs an IR gene expression program which is exacerbated during adipocyte differentiation. We propose that high glucose exposure conveys an epigenetic 'priming' of IR genes, favoring a transcriptional inflammatory response upon adipogenic stimulation. Chromatin alterations at IR genes by high glucose exposure may play a role in the etiology of metabolic diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 467, Issue 4, 27 November 2015, Pages 979-986
Journal: Biochemical and Biophysical Research Communications - Volume 467, Issue 4, 27 November 2015, Pages 979-986
نویسندگان
Torunn Rønningen, Akshay Shah, Andrew H. Reiner, Philippe Collas, Jan Ãivind Moskaug,