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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-09-0145v1 202/3/347    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Machado, M. Articles by Júnior, J. PubMed PubMed Citation Articles by Machado, M. Articles by Júnior, J.

M Machado, Departamento de Reprodução Animal e Radiologia Veterinária, Universidade Estadual Paulista, Botucatu, Brazil
V Portela, Centre de recherche en reproduction animale, Université de Montréal, St-Hyacinthe, Quebec, Canada
C Price, Centre de recherche en reproduction animale, Université de Montréal, St-Hyacinthe, Quebec, Canada
I da Costa, Reprodução Animal e Radiologia Veterinária, Universidade Estadual Paulista, Botucatu, Brazil
P Ripamonte, Fisiologia, Universidade Estadual Paulista, Botucatu, Brazil
R Amorim, Departamento de Clínica Veterinária, Universidade Estadual Paulista, Botucatu, Brazil
J Júnior, Fisiologia, Universidade Estadual Paulista, Botucatu, Brazil

Correspondence: Mariana Machado, Email: marifmach{at}ibb.unesp.br

Fibroblast growth factor 17 (FGF17) is a member of the FGF8 subfamily that appears to be relevant to folliculogenesis and oogenesis as the prototype member, FGF8, is an oocyte-derived protein that signals to cumulus cells. FGF8 has structural and receptor-binding similarities to FGF17, whose expression in the ovary has not been reported. In this study, we demonstrate localization of FGF17 protein to the oocyte of preantral follicles, and to the oocyte and granulosa cells of antral follicles. Real-time PCR demonstrated the presence of mRNA in oocytes and, to a lesser extent, in granulosa and theca cells. FGF17 mRNA abundance was low in granulosa and theca cells from healthy follicles and increased significantly in atretic follicles. Addition of FSH or IGF1 to granulosa cells in vitro decreased FGF17 mRNA abundance, and treatment with FGF17 inhibited estradiol and progesterone secretion from granulosa cells in relation to control cultures without these additives. We conclude that FGF17 is a potential mediator of granulosa cell differentiation.