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Published on: November 4, 2019
HIF-2 directly activates CD82 gene expression in endothelial cells
1Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan. kaorin@ri.ncvc.go.jp
Biochemical and Biophysical Research Communications
|March 9, 2011
Summary
Hypoxia-inducible factor 2 (HIF-2) specifically activates developmental genes in endothelial cells, unlike HIF-1. HIF-2 upregulates CD82, which inhibits cell migration, revealing a novel function for HIF-2.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Hypoxia-inducible factors (HIFs) regulate cellular responses to low oxygen.
- HIF-1 and HIF-2 share target genes but activate distinct subsets.
- Understanding differential gene activation is crucial for cellular function.
Purpose of the Study:
- To identify target genes preferentially activated by HIF-2 in endothelial cells.
- To compare the gene expression profiles induced by HIF-1 and HIF-2.
- To elucidate the specific functions regulated by HIF-2 in human umbilical vein endothelial cells (HUVECs).
Main Methods:
- DNA microarray analysis of HUVECs with forced expression of HIF-1α or HIF-2α.
- Comparative analysis of gene expression patterns.
- Functional assessment of CD82 in HUVECs.
Main Results:
- HIF-1 primarily induced glycolytic and metabolic genes.
- HIF-2 preferentially induced developmental genes, including Fms-like tyrosine kinase 1 (Flt-1) and angiopoietin 2 (Angpt2).
- HIF-2 upregulated CD82 expression by binding to its HRE consensus sequence, and CD82 was found to negatively regulate HUVEC cell migration.
Conclusions:
- HIF-2 plays a specific role in inducing developmental gene expression in endothelial cells.
- HIF-2-mediated induction of CD82 offers new insights into endothelial cell function and migration regulation.
- This study highlights the distinct roles of HIF-1 and HIF-2 in cellular responses to hypoxia.
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