Dynamics of the primate ovarian surface epithelium during the ovulatory menstrual cycle

Jay W. Wright, Leigh Jurevic, Richard Stouffer

    Research output: Contribution to journalArticle

    15 Citations (Scopus)

    Abstract

    BACKGROUND: Epithelial ovarian cancer (EOC) risk correlates strongly with the number of ovulations that a woman experiences. The primary source of EOC in women is the ovarian surface epithelium (OSE). Mechanistic studies on the etiology of OSE transformation to EOC cannot be realistically performed in women. Selecting a suitable animal model to investigate the normal OSE in the context of ovulation should be guided by the models reproductive similarities to women in natural features that are thought to contribute to EOC risk. Methods We selected the non-human primate, rhesus macaque, as a surrogate to study the normal OSE during the natural menstrual cycle. We investigated OSE morphology and marker expression, plus cell proliferation and death in relation to menstrual cycle stage and ovulation. Results OSE cells displayed a morphological range from squamous to columnar. Cycle-independent parameters and cycle-dependent changes were observed for OSE histology, steroid receptor expression, cell death, DNA repair and cell adhesion. Contrary to findings in non-primates, primate OSE cells were not manifestly cleared from the site of ovulation, nor were proliferation rates affected by ovulation or stage of the menstrual cycle. DNA repair proteins were more highly expressed in OSE than in other ovarian cells. CONCLUSIONS This study identifies significant differences between primate and non-primate OSE. In contrast to established views, ovulation-induced death and proliferation are not indicated as prominent contributors to EOC risk, but disruption of OSE cadherin-mediated adhesion may be, as could the loss of ovary-mediated chronic suppression of proliferation and elevation of DNA repair potential.

    Original languageEnglish (US)
    Pages (from-to)1408-1421
    Number of pages14
    JournalHuman Reproduction
    Volume26
    Issue number6
    DOIs
    StatePublished - Jun 2011

    Fingerprint

    Menstrual Cycle
    Primates
    Epithelium
    Ovulation
    DNA Repair
    Cell Death
    Steroid Receptors
    Cadherins
    Macaca mulatta
    Cell Adhesion
    Ovary
    Histology
    Animal Models
    Cell Proliferation
    Ovarian epithelial cancer

    Keywords

    • cadherin
    • epithelial ovarian cancer
    • menstrual cycle
    • non-human primate
    • ovarian surface epithelium

    ASJC Scopus subject areas

    • Rehabilitation
    • Obstetrics and Gynecology
    • Reproductive Medicine

    Cite this

    Dynamics of the primate ovarian surface epithelium during the ovulatory menstrual cycle. / Wright, Jay W.; Jurevic, Leigh; Stouffer, Richard.

    In: Human Reproduction, Vol. 26, No. 6, 06.2011, p. 1408-1421.

    Research output: Contribution to journalArticle

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    N2 - BACKGROUND: Epithelial ovarian cancer (EOC) risk correlates strongly with the number of ovulations that a woman experiences. The primary source of EOC in women is the ovarian surface epithelium (OSE). Mechanistic studies on the etiology of OSE transformation to EOC cannot be realistically performed in women. Selecting a suitable animal model to investigate the normal OSE in the context of ovulation should be guided by the models reproductive similarities to women in natural features that are thought to contribute to EOC risk. Methods We selected the non-human primate, rhesus macaque, as a surrogate to study the normal OSE during the natural menstrual cycle. We investigated OSE morphology and marker expression, plus cell proliferation and death in relation to menstrual cycle stage and ovulation. Results OSE cells displayed a morphological range from squamous to columnar. Cycle-independent parameters and cycle-dependent changes were observed for OSE histology, steroid receptor expression, cell death, DNA repair and cell adhesion. Contrary to findings in non-primates, primate OSE cells were not manifestly cleared from the site of ovulation, nor were proliferation rates affected by ovulation or stage of the menstrual cycle. DNA repair proteins were more highly expressed in OSE than in other ovarian cells. CONCLUSIONS This study identifies significant differences between primate and non-primate OSE. In contrast to established views, ovulation-induced death and proliferation are not indicated as prominent contributors to EOC risk, but disruption of OSE cadherin-mediated adhesion may be, as could the loss of ovary-mediated chronic suppression of proliferation and elevation of DNA repair potential.

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