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Hum. Reprod. Advance Access originally published online on November 13, 2007
Human Reproduction 2008 23(1):129-138; doi:10.1093/humrep/dem347
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© The Author 2007. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed: the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given: if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative word this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Induction of proliferation in the primate ovarian surface epithelium in vivo

Jay W. Wright1,5, Tanja Pejovic2,3, John Fanton4 and Richard L. Stouffer1,2

1 Division of Reproductive Sciences, Oregon National Primate Research Center, Beaverton, OR 97006, USA 2 Department of Obstetrics and Gynecology, Oregon Health and Science University, Portland, OR 97201, USA 3 Division of Gynecologic Oncology, Oregon Health and Science University, Portland, OR 97239, USA 4 Division of Animal Resources, Oregon National Primate Research Center, Beaverton, OR 97006, USA

5 Correspondence address. Tel: +1-503-690-5316; Fax: +1-503-690-5563; E-mail: wrightj{at}ohsu.edu

BACKGROUND: Epithelial ovarian cancer (EOC) is the primary ovarian malignancy affecting women. Proposed etiologies of EOC resist direct testing due to the absence of a suitable animal model, as EOC affects only primates, not other mammals. The role of proliferation in ovarian surface epithelium (OSE) transformation has been suggested but not demonstrated, nor has OSE proliferation been widely reported. We selected the rhesus macaque as a model to evaluate the unique primate OSE in vivo, and to determine whether it can undergo proliferative repair, which may relate to EOC etiology.

METHODS: Macaque ovaries were collected at three stages of the cycle. Very late luteal phase ovaries were gently brushed during laparoscopy to remove a portion of the OSE, and ovaries (≤3 per group) were collected 1–4 days later. Ovary samples were also collected from 10 women aged 33–74 years. Ovarian tissue sections were probed with OSE markers (keratin, β-catenin, E- and N-cadherin), proliferation markers [proliferating cell nuclear antigen (PCNA), phosphorylated histone H3 (phospho-H3), and phosphorylated Retinoblastoma (pRb)], or labels of collagen and basement membrane.

RESULTS: Brushing partially removed the OSE; did not cause tissue damage/adhesions; elevated the frequency of PCNA, phospho-H3 and pRb in the residual OSE, marking as many as 10–50% of cells in brushed regions (unbrushed areas contained <0.1% positive cells), and; did not induce proliferation in underlying stromal cells.

CONCLUSIONS: The OSE can undergo proliferative repair, and thus its normal regulation could contribute to EOC etiology.

Key words: epithelial ovarian cancer/ovarian surface epithelium/cell proliferation/ovarian malignancy/rhesus macaque

Submitted on April 6, 2007; resubmitted on September 25, 2007; accepted on October 4, 2007.


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