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Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

ABSTRACT: Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (HIF-2α) protein. In this study, we have attempted to explore the effects of HIF-2α overexpression on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE104794 | GEO | 2017/10/10

SECONDARY ACCESSION(S): PRJNA413831

REPOSITORIES: GEO

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Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

Project description:Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

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HIF-1α and HIF-2α differently regulate tumour development, metabolism and inflammation of clear cell renal cell carcinoma in mice

Project description:Mutational inactivation of VHL is the earliest genetic event in the majority of ccRCCs, leading to activation of the HIF-1α and HIF-2α transcription factors. While correlative studies of human ccRCCs and functional studies using human ccRCC cell lines have implicated HIF-1α as an inhibitor and HIF-2α as a promoter of aggressive tumour behaviours, their roles in tumour onset have not been functionally addressed. Using an autochthonous ccRCC model, we show genetically that Hif1a is necessary for tumour formation whereas Hif2a deletion has only minor effects on tumour initiation and growth. Both HIF-1α and HIF-2α are necessary for the clear cell phenotype. Transcriptomic and proteomic analyses revealed that HIF-1α regulates glycolysis while HIF-2α regulates genes associated with lipoprotein metabolism, ribosome biogenesis and E2F and MYC transcriptional activities. Deficiency of HIF-2α increased CD8+ T cell infiltration and activation. These studies reveal different functions of HIF-1α and HIF-2α in ccRCC. SIGNIFICANCE The roles of HIF-1α and HIF-2α in ccRCC pathogenesis remain unclear. Using a mouse genetic approach we show that HIF-1α but not HIF-2α is important for tumour formation, contrary to predictions from studies of human ccRCC. We show that HIF-1α and HIF-2α transcriptionally regulate different aspects of metabolism and identify HIF-2α as a suppressor of immune cell infiltration and activation.

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