کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10758519 1050408 2013 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hypoxia-induced regulation of the very low density lipoprotein receptor
ترجمه فارسی عنوان
تنظیم ناشی از هیپوکسی گیرنده لیپوپروتئین بسیار کم تراکم
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
چکیده انگلیسی
The very low density lipoprotein receptor (VLDLr) is highly upregulated during hypoxia in mouse cardiomyocytes and in human and mouse ischemic hearts causing a detrimental lipid accumulation. To know how the gene is regulated is important for future studies. In this study, we have thoroughly mapped the 5′-flanking region of the mouse VLDLr promoter and show that the hypoxia-mediated increase in VLDLr expression is dependent on Hif-1α binding to a hypoxia responsive element (HRE) located at −162 to −158 bp 5′of translation start. We show that classical HRE sites and the previously described PPARγ and Sp1 binding are not involved in the hypoxia-induced regulation of the VLDLr promoter. Using a chromatin immunoprecipitation (ChIP) assay, we show that Hif-1α specifically binds and activates the mouse VLDLr promoter at the previously described non-classical HRE in HL-1 cells. We also show that the same HRE is present and active in response to hypoxia in human cardiomyocytes, however at a different location (−812 bp from translation start). These results conclude that in the hypoxic hearts of mice and men, the VLDLr gene is regulated by a direct binding of Hif-1α to the VLDLr promoter.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 437, Issue 2, 26 July 2013, Pages 274-279
نویسندگان
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