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Open Access Publications from the University of California

Activation of Endoplasmic Reticulum Stress in Granulosa Cells from Patients with Polycystic Ovary Syndrome Contributes to Ovarian Fibrosis.

  • Author(s): Takahashi, Nozomi
  • Harada, Miyuki
  • Hirota, Yasushi
  • Nose, Emi
  • Azhary, Jerilee Mk
  • Koike, Hiroshi
  • Kunitomi, Chisato
  • Yoshino, Osamu
  • Izumi, Gentaro
  • Hirata, Tetsuya
  • Koga, Kaori
  • Wada-Hiraike, Osamu
  • Chang, R Jeffrey
  • Shimasaki, Shunichi
  • Fujii, Tomoyuki
  • Osuga, Yutaka
  • et al.

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Recent studies report the involvement of intra-ovarian factors, such as inflammation and oxidative stress, in the pathophysiology of polycystic ovary syndrome (PCOS), the most common endocrine disorder of reproductive age women. Endoplasmic reticulum (ER) stress is a local factor that affects various cellular events during a broad spectrum of physiological and pathological conditions. It may also be an important determinant of pro-fibrotic remodeling during tissue fibrosis. In the present study, we showed that ER stress was activated in granulosa cells of PCOS patients as well as in a well-established PCOS mouse model. Pharmacological inducers of ER stress, tunicamycin and thapsigargin, were found to increase the expression of pro-fibrotic growth factors, including transforming growth factor (TGF)-β1, in human granulosa cells, and their expression also increased in granulosa cells of PCOS patients. By contrast, treatment of PCOS mice with an ER stress inhibitor, tauroursodeoxycholic acid or BGP-15, decreased interstitial fibrosis and collagen deposition in ovaries, accompanied by a reduction in TGF-β1 expression in granulosa cells. These findings suggest that ER stress in granulosa cells of women with PCOS contributes to the induction of pro-fibrotic growth factors during ovarian fibrosis, and that ER stress may serve as a therapeutic target in PCOS.

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