Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of rat testis aafter acute antibody mediated FSH suppression

ABSTRACT: To unravel the genes that underpin the effects of FSH on spermatogenesis, testicular gene expression was compared in juvenile rats after FSH suppression to littermate controls. Based on existing data, it is apparent that the dominant function of FSH shifts between 9 and 18 day postpartum (dpp) during the first wave of spermatogenesis from driving Sertoli cell proliferation to support of germ cells. To enable comprehensive analysis of the impact of acute in vivo FSH suppression on Sertoli and germ cell development and to determine the genes that underpin these affects, FSH was selectively suppressed in Sprague Dawley rats by passive immunisation for 4 days prior to testis collection at 18 days postpartum. FSH suppression did not affect Sertoli cell proliferation at 18 dpp, but germ cell numbers were decreased at 18 dpp following FSH suppression, with a corresponding increase in germ cell apoptosis measured. Sixty transcripts were measured as changed at 18 dpp in response to 4 days of FSH suppression, as assessed using Affymetrixâ¢ microarrays. Some of these are known as Sertoli cell-derived FSH-responsive genes (e.g. StAR, cathepsin L, insulin-like growth factor binding protein-3), while others encode proteins involved in cell cycle and survival regulation (e.g. cyclin D1, scavenger receptor class B 1). These data demonstrate that FSH affects germ cells in vivo, by supporting germ cell viability at day 18. This model enabled identification of candidate genes that contribute to the FSH-mediated pathway by which Sertoli cells support germ cells. Experiment Overall Design: Sprague Dawley male rats at day 14 postpartum received either a rat FSH antibody raised in sheep or a control sheep immunoglobulin for 4 days. RNA was extracted from the testis and hybridisation on Affymetrix microarrays was conducted.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Michael Skinner

PROVIDER: E-GEOD-10293 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation.

Meachem Sarah J SJ Ruwanpura Saleela M SM Ziolkowski Jessica J Ague Jacquelyn M JM Skinner Michael K MK Loveland Kate L KL

The Journal of endocrinology 20050901 3

The critical influence of follicle stimulating hormone (FSH) on male fertility relates both to its impact on Sertoli cell proliferation in perinatal life and to its influence on the synthesis of Sertoli cell-derived products essential for germ cell survival and function in the developing adult testis. The nature and timing of this shift of germ cells to their reliance on specific Sertoli cell-derived products are not defined. Based on existing data, it is apparent that the dominant function of F ...[more]

PMID: 16135663

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Project description:Fsh-mediated regulation of zebrafish spermatogenesis includes modulating the expression of testicular growth factors. Here, we study if and how two Sertoli cell-derived Fsh-responsive growth factors, anti-Müllerian hormone (Amh; inhibiting steroidogenesis and germ cell differentiation) and insulin-like growth factor 3 (Igf3; stimulating germ cell differentiation), cooperate in regulating spermatogonial development. In dose response and time course experiments with primary testis tissue cultures, Fsh upregulated igf3 transcript levels and down-regulated amh transcript levels; igf3 transcript levels were more rapidly up-regulated and responded to lower Fsh concentrations than were required to decrease amh mRNA levels. Quantification of immunoreactive Amh and Igf3 on testis sections showed that Fsh increased slightly Igf3 staining but decreased clearly Amh staining. Studying the direct interaction of the two growth factors showed that Amh compromised Igf3-stimulated proliferation of type A (both undifferentiated [Aund] and differentiating [Adiff]) spermatogonia. Also the proliferation of those Sertoli cells associated with Aund spermatogonia was reduced by Amh. To gain more insight into how Amh inhibits germ cell development, we examined Amh-induced changes in testicular gene expression by RNA sequencing. The majority (69%) of the differentially expressed genes was down-regulated by Amh, including several stimulators of spermatogenesis, such as igf3 and steroidogenesis-related genes. At the same time, Amh increased the expression of inhibitory signals, such as inha and id3, or facilitated prostaglandin E2 (PGE2) signaling. Evaluating one of the potentially inhibitory signals, we indeed found in tissue culture experiments that PGE2 promoted the accumulation of Aund at the expense of Adiff and B spermatogonia. Our data suggest that an important aspect of Fsh bioactivity in stimulating spermatogenesis is implemented by restricting the different inhibitory effects of Amh and by counterbalancing them with stimulatory signals, such as Igf3

Dataset Information

Transcription profiling of rat testis aafter acute antibody mediated FSH suppression

Publications

Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation.

Similar Datasets

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