An Autoradiographic Study of Rabbit Ovarian Surface Epithelium Before and After Ovulation1

Osterholzer, Heinz O.; Johnson, Joseph R.; Nicosia, Santo V.

doi:10.1095/biolreprod33.3.729

Cited by 50 publications

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“…In addition, both FSH and hCGlike hormones increase KL mRNA expression in granulosa cells of mice (Motro and Bernstein, 1993) and rats (Ismail et al, 1996). Although there is evidence that OSE cells express receptors for both LH (Osterholzer et al, 1985) and FSH (Zheng et al, 1996), the immortalized OSE cell line used in this study does not express these receptors (manuscript in preparation). However, cAMP serves as the second messenger following receptor activation by both gonadotropins, and activation of this signalling pathway can be mimicked by dbcAMP.…”

Section: Discussionmentioning

confidence: 84%

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

1999

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In preparation for ovulation, paracrine communication between the preovulatory follicle and overlying theca/ stromal cells and ovarian surface epithelium (OSE) must take place to facilitate the degradative and apoptotic events associated with ovulation. Kit tyrosine kinase receptors and their ligand, kit ligand (KL) are expressed within ovarian follicles, and ligand-induced receptor activation appears to account for some of the cell ± cell interactions important for oocyte development. We investigated the expression of Kit receptors and KL in OSE cells and the possibility that modulation of their expression could a ect OSE cell activity. KL mRNA and protein were detected in the OSE cell layer of rat ovaries, and primary cultures of rat OSE as well as the immortalized rat OSE cell line, ROSE 199, expressed KL, but not Kit receptors. Both primary and immortalized OSE cells preferentially expressed KL-1, rather than KL-2, transcripts, suggesting that these cells produce predominantly the soluble form of KL. Activation of the cAMP signalling pathway using dibutyryl cAMP decreased proliferation of ROSE 199 cells and elicited a threefold increase in KL expression. TGF-b similarly inhibited ROSE 199 cell proliferation, but strongly inhibited dibutyryl cAMP-induced KL expression, indicating that changes in KL expression were not directly associated with OSE cell proliferation. The expression of mostly soluble KL in the surface epithelium suggests that this cytokine may be acting in a paracrine fashion, perhaps interacting with nearby Kit receptorbearing theca cells.

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Section: Discussionmentioning

confidence: 84%

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

1999

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“…Normal human OSE express specific receptors for FSH and LH/hCG both in vivo and in vitro (42)(43)(44). However, the findings regarding the effect of FSH and LH/hCG on OSE are inconsistent; treatment with gonadotropins stimulated OSE proliferation in some studies (43,(45)(46)(47) but was either noneffective (16) or inhibitory for other cases (48). In this study, we observed changes in N-cadherin levels at concentrations of FSH that correlate with the profile of serum concentration of FSH and LH/hCG in the normal reproductive cycle.…”

Section: Inhibitor Of Matrix Metalloproteinase Inhibits the Camp-medimentioning

confidence: 99%

Gonadotropins Regulate N-cadherin-mediated Human Ovarian Surface Epithelial Cell Survival at Both Post-translational and Transcriptional Levels through a Cyclic AMP/Protein Kinase A Pathway

Pon

Auersperg

Wong

2005

Journal of Biological Chemistry

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Gonadotropins are the major regulators of ovarian function and may be involved in the etiology of ovarian cancer. In this study, we report a new mechanism whereby gonadotropins regulate the survival of human ovarian surface epithelium (OSE), the tissue of origin of epithelial ovarian carcinomas. Our results indicate that disruption of N-cadherin-mediated cell-cell adhesion is an important molecular event in the apoptosis of human OSE. Treatment with surge serum concentrations of gonadotropins reduced the amount of N-cadherin with a concomitant induction of apoptosis, and this effect was mediated by a cAMP/protein kinase A pathway but not the ERK1/2 and protein kinase C cascades. We further demonstrated that activation of the gonadotropins/ cAMP signaling pathway in human OSE led to a rapid down-regulation of N-cadherin protein level followed by a reduction at the level of N-cadherin mRNA, indicating that expression of N-cadherin was regulated by posttranslational and transcriptional mechanisms. The former mechanism was mediated by increased turnover of N-cadherin protein and could be reversed by inhibition of proteasomal or matrix metalloproteinase (MMP-2) activity. On the other hand, at the transcriptional level, the addition of actinomycin D abolished the cAMP-mediated decrease in N-cadherin mRNA but did not change its stability. Inhibition of protein kinase A or expressing a dominant negative mutant of cAMP-response elementbinding protein blocked this decrease of N-cadherin mRNA. Together, the combined operation of post-translational and transcriptional mechanisms suggests that regulation of N-cadherin is a crucial event and emphasizes the important role that N-cadherin has in controlling the survival capability of human OSE.The surface of the human ovary is covered with a single layer of flat-to-cuboidal mesothelial cells, the ovarian surface epithelium (OSE).1 During each reproductive cycle, the OSE takes part in the cyclical ovulatory ruptures and repair. OSE on the preovulatory follicle undergoes apoptosis at the time of ovulation and then proliferates rapidly to repair the ruptured follicle and reconstitutes an intact mesothelium (1). However, factors regulating cell death and growth in human OSE are poorly understood. Because OSE is the source of epithelial ovarian carcinomas, which is the leading cause of death among all the human gynecological neoplasms, understanding the mechanisms that regulate OSE cell survival, apoptosis, and cell growth is of great clinical importance because an aberrant signaling of any of these pathways is likely to be involved in epithelial ovarian cancer. The cadherins are a family of cell surface glycoproteins that function in promoting calcium-dependent cell-cell adhesion and play crucial roles in the maintenance of structure, differentiation, and function of reproductive tissues (reviewed in Ref. 2). In general, cadherins are expressed in a cell-specific manner within specific compartments of the ovary, and their expression shows changes during different differentiation or...

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“…Prior to ovulation, OSE proliferation increases at sites adjacent to follicular development (Bjersing & Cajander 1974, Burdette et al 2006) and ovulationrelated desquamation of the surface epithelial cells involves programmed cell death or apoptosis (Bjersing & Cajander 1975, Ackerman & Murdoch 1993, Murdoch 1994, 1995. Following ovulation, the wound at the ovarian surface is rapidly repaired by proliferation of the OSE from the perimeter of the ruptured follicle, and ovarian epithelial cells have also been postulated to be involved in the deposition and restructuring of the extracellular matrix of the tunica albuginea (Motta 1980, Osterholzer et al 1985, Kruk & Auersperg 1992, Gaytan et al 2005, Burdette et al 2006. The constant rounds of proliferation and repair following ovulation provide the opportunity for replication errors and dysregulation of the genes involved in the normal processes of proliferation, apoptosis, and DNA repair, and thus may contribute to neoplastic progression in the OSE (Fathalla 1971).…”

Section: Introductionmentioning

confidence: 99%

Global gene expression profiles of ovarian surface epithelial cells in vivo

Gava

Bye

deFazio

2008

Journal of Molecular Endocrinology

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Epithelial ovarian cancer, the leading cause of death from gynecological malignancy in Western countries, is thought to arise from the ovarian surface epithelium (OSE). It has been postulated that the constant rounds of proliferation and repair following ovulation contributes to neoplastic transformation. However, there is little information on the genes and pathways which are involved in the normal functions of the ovarian epithelium, in particular genes that are hormone responsive and those central to functions such as proliferation and apoptosis during ovulation. We used laser microdissection and cDNA microarrays to profile gene expression specifically in mouse ovarian epithelial cells, first compared with other ovarian cells, and secondly between ovarian epithelium collected at different physiological stages. We identified over 1000 transcripts that were consistently more highly expressed in the ovarian epithelium compared with remaining ovarian cell types, including genes involved in cell growth, transcription, and cell adhesion. At the various physiological stages examined, the highest number of regulated genes was found during the estrous cycle, specifically on the evening of proestrus, coincident with the ovulatory surge of hormones and just prior to ovulation. The expression of several selected genes, identified by the microarray analysis, including Villin 2, Keratin 8, Arginine-rich mutated in epithelial tumors, and Tumor-associated calcium signal transducer 1, was validated by independent methods. The identification of genes expressed and regulated in the OSE, and characterization of the pathways involved, will contribute to a more detailed understanding of the ovarian epithelium transcriptome and ultimately lead to a better understanding of the aberrations leading to malignant transformation in the ovarian epithelium.

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An Autoradiographic Study of Rabbit Ovarian Surface Epithelium Before and After Ovulation1

Cited by 50 publications

References 0 publications

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

Gonadotropins Regulate N-cadherin-mediated Human Ovarian Surface Epithelial Cell Survival at Both Post-translational and Transcriptional Levels through a Cyclic AMP/Protein Kinase A Pathway

Global gene expression profiles of ovarian surface epithelial cells in vivo

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