Linkage of regulators of TGF-β activity in the fetal ovary to polycystic ovary syndrome

Nicholas Hatzirodos, Rosemary A. Bayne, Helen F. Irving-Rodgers, Katja Hummitzsch, Laetitia Sabatier, Sam Lee, Wendy Bonner, Mark A. Gibson, William E. Rainey, Bruce R. Carr, Helen D. Mason, Dieter P. Reinhardt, Richard A. Anderson, Raymond J. Rodgers

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


Although not often discussed, the ovaries of women with polycystic ovary syndrome (PCOS) show all the hallmarks of increased TGF-β activity, with increased amounts of fibrous tissue and collagen in the ovarian capsule or tunica albuginea and ovarian stroma. Recent studies suggest that PCOS could have fetal origins. Genetic studies of PCOS have also found linkage with a microsatellite located in intron 55 of the extracellular matrix protein fibrillin 3. Fibrillins regulate TGF-β bioactivity in tissues by binding latent TGF-β binding proteins. We therefore examined expression of fibrillins 1-3, latent TGF-β binding proteins 1-4, and TGF-β 1-3 in bovine and human fetal ovaries at different stages of gestation and in adult ovaries. We also immunolocalized fibrillins 1 and 3. The results indicate that TGF-β pathways operate during ovarian fetal development, but most important, we show fibrillin 3 is present in the stromal compartments of fetal ovaries and is highly expressed at a critical stage early in developing human and bovine fetal ovaries when stroma is expanding and follicles are forming. These changes in expression of fibrillin 3 in the fetal ovary could lead to a predisposition to develop PCOS in later life.

Original languageEnglish (US)
Pages (from-to)2256-2265
Number of pages10
JournalFASEB Journal
Issue number7
StatePublished - Jul 2011


  • Fibrillin
  • Latent transforming growth factor-β binding protein

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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