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Published in: Endocrine 2/2015

01-03-2015 | Original Article

Mouse GDF9 decreases KITL gene expression in human granulosa cells

Authors: Astrud R. Tuck, David G. Mottershead, Herman A. Fernandes, Robert J. Norman, Wayne D. Tilley, Rebecca L. Robker, Theresa E. Hickey

Published in: Endocrine | Issue 2/2015

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Abstract

Kit ligand (KITL) is an important granulosa cell-derived growth factor in ovarian folliculogenesis, but its expression and function in human granulosa cells are currently poorly understood. Based on studies performed in animal models, it was hypothesised that KITL gene expression in human granulosa cells is regulated by androgens and/or growth differentiation factor 9 (GDF9). We utilised two models of human granulosa cells, the KGN granulosa tumour cell line and cumulus granulosa cells obtained from preovulatory follicles of women undergoing assisted reproduction. Cells were treated with combinations of 5α-dihydrotestosterone (DHT), recombinant mouse GDF9, and the ALK4/5/7 inhibitor SB431542. KITL mRNA levels were measured by quantitative real-time PCR. No change in KITL mRNA expression was observed after DHT treatment under any experimental conditions, but GDF9 treatment resulted in a significant decrease in KITL mRNA levels in both KGN and cumulus cells. The effect of GDF9 was abolished by the addition of SB431542. These results indicate that KITL is not directly regulated by androgen signalling in human granulosa cells. Moreover, this study provides the first evidence that GDF9 negatively regulates KITL gene expression in human granulosa cells providing new information on the regulation of these important growth factors in the human ovary.
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Metadata
Title
Mouse GDF9 decreases KITL gene expression in human granulosa cells
Authors
Astrud R. Tuck
David G. Mottershead
Herman A. Fernandes
Robert J. Norman
Wayne D. Tilley
Rebecca L. Robker
Theresa E. Hickey
Publication date
01-03-2015
Publisher
Springer US
Published in
Endocrine / Issue 2/2015
Print ISSN: 1355-008X
Electronic ISSN: 1559-0100
DOI
https://doi.org/10.1007/s12020-014-0335-6

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