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Effects of FSH on testicular mRNA transcript levels in the hypogonadal mouse

ABSTRACT: In the normal mouse the pituitary gonadotrophins determine development, maturation and physiological regulation of the testis with follicle-stimulating hormone (FSH) activating the Sertoli cell and luteinising hormone (LH) the Leydig cell. To look at the potential interaction of cell types within the testis following hormone stimulation we have investigated the effect of rFSH on testicular gene expression in the hypogonadal (hpg) male mouse. Due to a deletion in the gene encoding gonadotrophin-releasing hormone (GnRH), FSH and LH levels are at the lower limit of detection in the circulation and mice remain in a pre-pubertal state throughout life unless given exogenous hormone. Here we have addressed important question of changes in the global gene expression profile of testicular tissue following hormone stimulation (rFSH) for 12, 24 and 72h following injections compared to control untreated hpg males of the same age. Keywords: Hormone Response, Testicular gene expression Profile

ORGANISM(S): Mus musculus

PROVIDER: GSE8924 | GEO | 2009/08/18

SECONDARY ACCESSION(S): PRJNA102333

REPOSITORIES: GEO

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Project description:We recently demonstrated that Fsh modifies in vitro the testicular transcriptome of rainbow trout at early stages of spermatogenesis. Some of the regulated genes were found related to pathways highly relevant for the testicular functions i.e. spermatogenesis and steroidogenesis. Unlike in mammals, in fish both gonadotropins are able to efficiently stimulate the steroidogenesis, likely through a direct interaction with their cognate receptors present on the Leydig cells. In this context, we wondered whether the effects of Fsh on the tubular compartment were mediated through the production of steroids. To address this issue we performed in vitro incubations of testis explants in the presence of Fsh alone or in combination with an inhibitor of the steroidogenesis, the trilostane. Trilostane significantly reduced or suppressed the response to Fsh of many genes showing that important aspects of the Fsh action on fish testis is indirect and requires the production of steroids. Interestingly, most of the genes regulated in response to Fsh through the steroid mediation were similarly regulated by Lh and many were also found regulated by androgen treatment. On the other hand, for many other genes the response to Fsh was not affected in the presence of trilostane. A majority of those genes were also preferentially regulated by Fsh, as compared to Lh, suggesting that specific regulatory effects of Fsh were independent of steroid production. Finally antagonistic effects between Fsh and steroids were found, in particular for genes encoding clue factors of steroidogenesis or for genes of the Igf system that tended to be inhibited by androgens. Testes were collected from all-male population rainbow trout at early stages of spermatogenesis.Testes were chopped in small pieces, in sterile conditions and then pooled and mixed. Testis fragments were randomly distributed (60-80 mg per well) on Nunc polycarbonate membrane inserts in 24-well plates filled with 300 ÂµL of modified L15 culture medium supplemented with 2% Ultroser SF. Incubation were performed in six replicates for 96 hours, at 12Â°C, in the absence or presence of purified trout Fsh alone (500 ng/mL) or in combination with 10 Âµg/mL trilostane, an inhibitor of 3 beta-hydroxysteroid dehydrogenase. A pre-incubation with trilostane was done for 1 hour before adding Fsh.

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Effects of FSH on testicular mRNA transcript levels in the hypogonadal mouse

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