Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 345390
Title Luteinizing hormone inhibits Fas-induced apoptosis in ovarian surface epithelial cell lines
Author(s) Slot, K.A.; Boer-Brouwer, M. de; Houweling, M.; Vaandrager, A.B.; Dorrington, J.H.; Teerds, K.J.
Source Journal of Endocrinology 188 (2006)3. - ISSN 0022-0795 - p. 227 - 239.
DOI https://doi.org/10.1677/joe.1.06087
Department(s) Human and Animal Physiology
WIAS
Publication type Refereed Article in a scientific journal
Publication year 2006
Keyword(s) follicle-stimulating-hormone - growth-factor-i - protein-kinase-a - granulosa-cells - cancer-cells - cyclic-amp - gonadotropin receptor - gene-expression - neutrophil apoptosis - incessant ovulation
Abstract Gonadotrophins including LH have been suggested to play an important role in the etiology of epithelial ovarian cancers. The goal of the present study was to obtain more insight in the mechanism of gonadotrophin action on ovarian surface epithelium (OSE) cells. As the Fas system is known to be a major player in the regulation of the process of apoptosis in the ovary, we investigated whether LH interfered with Fas-induced apoptosis in the human OSE cancer cell lines HEY and Caov-3. Activation of Fas receptor by an agonistic anti-Fas receptor antibody induced apoptosis, as was evaluated by caspase-3 activation, poly(ADP-ribose) polymerase fragmentation, phosphatidylserine externalization and morphological changes characteristic of apoptosis. Co-treatment with LH reduced the number of apoptotic cells following activation of Fas in a transient manner, while LH by itself did not affect apoptosis or cell proliferation. The anti-apoptotic effect of LH could be mimicked by the membrane-permeable cAMP analog 8-(4-chlorophenylthio) cAMP (8-CPT-cAMP), and blocked by H89, a specific inhibitor of protein kinase A (PKA). In conclusion, these findings suggest that LH protects HEY cells against Fas-induced apoptosis through a signaling cascade involving PKA. Although it is plausible that in vivo LH might also enhance OSE tumor growth through inhibition of apoptosis, further research is necessary to confirm this hypothesis.
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