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http://purl.uniprot.org/citations/18658046http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18658046http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18658046http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Hypoxia-inducible factor 1alpha (HIF-1alpha) is primarily involved in the adapting of cells to changes in oxygen levels, which is essential for normal vascular function. Recently, physiological roles for retinoic acid-related orphan receptor alpha (RORalpha) have been implicated in cardiovascular diseases such as atherosclerosis. In this study, we have investigated the potential roles of RORalpha in the hypoxia signaling pathway in connection with activation of HIF-1alpha.

Methods and results

Under hypoxic conditions, expression of RORalpha was induced. When RORalpha was introduced exogenously, protein level as well as transcriptional activity of HIF-1alpha was enhanced. Putative ligands of RORalpha, such as melatonin and cholesterol sulfate, induced transcriptional activity for HIF-1alpha, which was abolished by RNA interference against RORalpha. RORalpha was physically associated with HIF-1alpha through DNA binding domain, which was required to the RORalpha-induced stabilization and transcriptional activation of HIF-1alpha. Finally, either infection with adenovirus encoding RORalpha or treatment with ROR ligands enhanced the formation of capillary tubes by human umbilical vascular endothelial cells.

Conclusions

Our results provide a new insight for the function of RORalpha in amplification of hypoxia signaling and suggest a potential application of RORalpha ligands for the therapy of hypoxia-associated vascular diseases."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.org/dc/terms/identifier"doi:10.1161/atvbaha.108.171546"xsd:string
http://purl.uniprot.org/citations/18658046http://purl.org/dc/terms/identifier"doi:10.1161/atvbaha.108.171546"xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lee I.K."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lee I.K."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lim Y.S."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lim Y.S."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Kim E.J."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Kim E.J."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lee M.O."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Lee M.O."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Na T.Y."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Na T.Y."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Yoo Y.G."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Yoo Y.G."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Yang W.K."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/author"Yang W.K."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/name"Arterioscler. Thromb. Vasc. Biol."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/name"Arterioscler. Thromb. Vasc. Biol."xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/pages"1796-1802"xsd:string
http://purl.uniprot.org/citations/18658046http://purl.uniprot.org/core/pages"1796-1802"xsd:string
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