Crosstalk between FSH and relaxin at the end of the proliferative stage of rat Sertoli cells

Crosstalk between FSH and relaxin at the end of the proliferative stage of rat Sertoli cells

Author Nascimento, Aline Rosa Autor UNIFESP Google Scholar
Macheroni, Carla Autor UNIFESP Google Scholar
Lucas, Thais Fabiana Gameiro Autor UNIFESP Google Scholar
Porto, Catarina Segreti Autor UNIFESP Google Scholar
Lazari, Maria de Fatima Magalhaes Autor UNIFESP Google Scholar
Abstract Follicle-stimulating hormone (FSH) stimulates the proliferation of immature Sertoli cells through the activation of PI3K/AKT/mTORC1 and MEK/ERK1/2 pathways. Mature Sertoli cells stop proliferating and respond to FSH by stimulating cAMP production. To gain insight into possible mechanisms involved in this switch as well as the impact of paracrine factors that stimulate cell proliferation, we analyzed the effects of FSH and relaxin on intracellular signaling pathways involved with proliferation and differentiation in Sertoli cells from 15-day-old rats, which are close to the transition between the two stages. FSH stimulated H-3-thymidine incorporation and cyclin D1 expression, changes associated with proliferation. In contrast, FSH inhibited AKT and ERK1/2 phosphorylation, activated cAMP production and induced changes in several cell cycle genes that were compatible with differentiation. Relaxin also stimulated 3H-thymidine incorporation but increased phosphorylation of ERK1/2 and AKT. When both hormones were added simultaneously, relaxin attenuated FSH-mediated inhibition of ERK1/2 and AKT phosphorylation and FSH-mediated activation of cAMP production. FSH but not relaxin increased CREB phosphorylation, and relaxin but not FSH shifted NF-kappa B expression from the cytoplasm to the nucleus. Relaxin did not inhibit the effects of FSH on inhibin alpha and Bcl2 expression. We propose that at this time of Sertoli cell development, FSH starts to direct cells to differentiation through activation of cAMP/CREB and inhibition of ERK1/2 and AKT pathways. Relaxin counteracts FSH signaling through the inhibition of cAMP and activation of ERK1/2, AKT and NF-kappa B, but does not block the differentiation process triggered by FSH.
xmlui.dri2xhtml.METS-1.0.item-coverage Bristol
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)/PNPD
Grant number FAPESP: 2010/10274-2
FAPESP: 2014/08563-7
FAPESP: 2011/14262-1
FAPESP: 2014/05028-3
CAPES/PNPD: 2745/2010
Date 2016
Published in Reproduction. Bristol, v. 152, n. 6, p. 613-628, 2016.
ISSN 1470-1626 (Sherpa/Romeo, impact factor)
Publisher Bioscientifica Ltd
Extent 613-628
Origin http://dx.doi.org/10.1530/REP-16-0330
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000387771600010
URI https://repositorio.unifesp.br/handle/11600/56685

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