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Hypoxia-induced reg...
Hypoxia-induced regulation of the very low density lipoprotein receptor
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- Perman Sundelin, Jeanna (author)
- Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberg Laboratory,Institute of Medicine, Department of Molecular and Clinical Medicine
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- Lidberg, Ulf, 1962 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
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- Nik, Ali Moussavi (author)
- Gothenburg University,Göteborgs universitet,Institutionen för kemi och molekylärbiologi,Department of Chemistry and Molecular Biology
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- Carlsson, Peter, 1959 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för kemi och molekylärbiologi,Department of Chemistry and Molecular Biology
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- Borén, Jan, 1963 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
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(creator_code:org_t)
- Elsevier BV, 2013
- 2013
- English.
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In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 0006-291X. ; 437:2, s. 274-279
- Related links:
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Abstract
Subject headings
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- 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-1 alpha, 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 PPAR gamma 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-1 alpha t 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-1 alpha to the VLDLr promoter. (C) 2013 Elsevier Inc. All rights reserved.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine (hsv//eng)
Keyword
- Very low density lipoprotein receptor
- Hypoxia inducible factor 1 alpha
- Hypoxia responsive element
- TRANSCRIPTIONAL REGULATION
- ADIPOCYTE DIFFERENTIATION
- BINDING PROTEIN
- MESSENGER-RNA
- EXPRESSION
- GENE
- ACTIVATION
- PROMOTER
- ELEMENTS
- ENHANCER
- KAHASHI S
- 1992
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
Publication and Content Type
- ref (subject category)
- art (subject category)
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