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Contribution of hypoxia‐inducible factor‐1α to transcriptional regulation of vascular endothelial growth factor in bovine developing luteal cells
Author(s) -
ZHANG Zhenghong,
YIN Dingzhong,
WANG Zhengchao
Publication year - 2011
Publication title -
animal science journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.606
H-Index - 38
eISSN - 1740-0929
pISSN - 1344-3941
DOI - 10.1111/j.1740-0929.2010.00832.x
Subject(s) - vascular endothelial growth factor , angiogenesis , hypoxia (environmental) , messenger rna , hypoxia inducible factors , vascular endothelial growth factor a , biology , gene expression , transfection , microbiology and biotechnology , chemistry , endocrinology , medicine , cancer research , gene , vegf receptors , biochemistry , organic chemistry , oxygen
ABSTRACT Vascular endothelial growth factor (VEGF)‐dependent angiogenesis is crucial for corpus leteum formation and their functional maintenance in mammalian ovaries. The present study was designed to test the hypothesis that hypoxia‐inducible factor (HIF)‐1α‐mediated transcriptional activation contributes to the increased expression of VEGF gene in response to hypoxia in the bovine developing luteal cells (LCs). By real‐time RT‐PCR analysis, VEGF messenger RNA (mRNA) expression was found to significantly increase under hypoxia or treatment with desferrioxamine (DFX), cobalt chloride (CoCl 2 ) or even N‐carbobenzoxyl‐L‐leucinyl‐L‐leucinyl‐L‐norvalinal (MG‐132), while these increased VEGF mRNA expressions could also be blocked by ferrous ammonium sulfate (FAS) or cis ‐element oligodeoxynucleotide (dsODN) transfection under hypoxia. Further analysis also found that these changes of VEGF mRNA were consistent with HIF‐1α expression or HIF‐1 activity. Taken together, our results indicate that VEGF is transcriptionally activated by hypoxia through HIF‐1α‐mediated mechanisms in LCs. This hypoxia‐induced transcriptional activation may be one of the important mechanisms mediating the increase of VEGF expression in developing LCs during mammalian corpus leteum formation.