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Hormonally regulated follicle differentiation and luteinization in the mouse is associated with hypoxia inducible factor activity

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dc.contributor.authorTam, K.
dc.contributor.authorRussell, D.
dc.contributor.authorPeet, D.
dc.contributor.authorBracken, C.
dc.contributor.authorRodgers, R.
dc.contributor.authorThompson, J.
dc.contributor.authorKind, K.
dc.date.issued2010
dc.description.abstractHypoxia inducible factors (HIFs) are transcription factors that mediate physiological responses to hypoxia Hypoxia is established as the major inducer of HIFs, but stimuli such as transition metals and hormones also induce HIF target genes Whilst the ovarian granulosa cell layer is known to be avascular and the follicle is vascularised via the thecal cell layer, little is known about the role of hypoxia or HIFs in regulating ovarian function In this study, we hypothesized that hypoxia as well as non-hypoxic stimuli cooperate in promoting follicle differentiation and luteinization via HIF activity and resultant gene regulation. We quantitatively measured the HIFI a protein response to hCG in ovarian granulosa cell cultures and in vivo and developed a transgenic(HRE(4)-SV40-EGFP)HIF reporter mouse line We observed a time-dependent increase of HIFI a protein levels in granulosa cells post-hCG in vivo, maximal around time of ovulation hCG alone was unable to promote HIF1 alpha protein accumulation in cultured granulosa cells, but increased protein abundance was observed when combined with a hypoxic stimulus. HRE-EGFP ovaries showed no follicular EGFP in stages prior to antrum formation. However, HIF regulated EGFP was maximally induced in granulosa cells around the time of ovulation and readily observed in corpora lutea. There was also an increase in HIF regulated EGFP activity in the corpora lutea from functional to regressing stages. Taken together, these observations establish the notion that HIFs play a role during follicular differentiation and luteinization.
dc.description.statementofresponsibilityKimberley K.Y. Tam, Darryl L. Russell, Daniel J. Peet, Cameron P. Bracken, Raymond J. Rodgers, Jeremy G. Thompson, and Karen L. Kind
dc.identifier.citationMolecular and Cellular Endocrinology, 2010; 327(1-2):47-55
dc.identifier.doi10.1016/j.mce.2010.06.008
dc.identifier.issn0303-7207
dc.identifier.issn1872-8057
dc.identifier.orcidRussell, D. [0000-0002-4930-7658]
dc.identifier.orcidPeet, D. [0000-0002-6085-8936]
dc.identifier.orcidRodgers, R. [0000-0002-2139-2969]
dc.identifier.orcidThompson, J. [0000-0003-4941-7731]
dc.identifier.urihttp://hdl.handle.net/2440/60690
dc.language.isoen
dc.publisherElsevier Sci Ireland Ltd
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/453556
dc.rightsCopyright © 2010 Elsevier Ireland Ltd. All rights reserved.
dc.source.urihttps://doi.org/10.1016/j.mce.2010.06.008
dc.subjectFollicle
dc.subjectOvulation
dc.subjectHuman chorionic gonadotropin
dc.subjectHypoxia inducible factor
dc.titleHormonally regulated follicle differentiation and luteinization in the mouse is associated with hypoxia inducible factor activity
dc.typeJournal article
pubs.publication-statusPublished

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