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• W2009283014 abstract "• The VLDLr promoter activity is regulated by a non-classical hypoxia responsive element (HRE). • The binding of Hif-1α to the VLDLr promoter is specific for both mouse and human cardiomyocytes. • The active HRE site is conserved but located at different positions in humans. 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." @default.
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• W2009283014 date "2013-07-01" @default.
• W2009283014 modified "2023-09-24" @default.
• W2009283014 title "Hypoxia-induced regulation of the very low density lipoprotein receptor" @default.
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• W2009283014 doi "https://doi.org/10.1016/j.bbrc.2013.06.066" @default.
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