Gene expression profiling of mouse Sertoli cell lines

Strothmann, K; Simoni, Manuela; Mathur, Premendu P.; Siakhamary, Susan; Nieschlag, Eberhard; Gromoll, Jörg

doi:10.1007/s00441-003-0834-x

Cited by 14 publications

(15 citation statements)

References 46 publications

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“…We have used a transgenic approach to rescue the lethality by crossing with the K14-Cdk2ap1 transgenic mice. It is well documented that K14 promoter is active in epithelial tissues, including skin, palate, tongue, and ovary [35], [36], [37], [38], [39], [40]. In the previous paper demonstrating the phenotype of K14-Cdk2ap1 mice, we have observed the overexpression of Cdk2ap1 in epithelial tissues [12].…”

Section: Discussionmentioning

confidence: 49%

Targeted Inactivation of p12Cdk2ap1, CDK2 Associating Protein 1, Leads to Early Embryonic Lethality

et al. 2009

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Targeted disruption of murine Cdk2ap1, an inhibitor of CDK2 function and hence G1/S transition, results in the embryonic lethality with a high penetration rate. Detailed timed pregnancy analysis of embryos showed that the lethality occurred between embryonic day 3.5 pc and 5.5 pc, a period of implantation and early development of implanted embryos. Two homozygous knockout mice that survived to term showed identical craniofacial defect, including a short snout and a round forehead. Examination of craniofacial morphology by measuring Snout Length (SL) vs. Face Width (FW) showed that the Cdk2ap1+/− mice were born with a reduced SL/FW ratio compared to the Cdk2ap1+/+ and the reduction was more pronounced in Cdk2ap1−/− mice. A transgenic rescue of the lethality was attempted by crossing Cdk2ap1+/− animals with K14-Cdk2ap1 transgenic mice. Resulting Cdk2ap1+/−:K14-Cdk2ap1 transgenic mice showed an improved incidence of full term animals (16.7% from 0.5%) on a Cdk2ap1−/− background. Transgenic expression of Cdk2ap1 in Cdk2ap1−/−:K14-Cdk2ap1 animals restored SL/FW ratio to the level of Cdk2ap1+/−:K14-Cdk2ap1 mice, but not to that of the Cdk2ap1+/+:K14-Cdk2ap1 mice. Teratoma formation analysis using mESCs showed an abrogated in vivo pluripotency of Cdk2ap1−/− mESCs towards a restricted mesoderm lineage specification. This study demonstrates that Cdk2ap1 plays an essential role in the early stage of embryogenesis and has a potential role during craniofacial morphogenesis.

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Section: Discussionmentioning

confidence: 49%

Targeted Inactivation of p12Cdk2ap1, CDK2 Associating Protein 1, Leads to Early Embryonic Lethality

et al. 2009

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“…References for those genes previously reported to be in the rat testis and/or regulated by FSH are in parentheses. Yes; (Walker et al 1994, West et al 1994, Monaco et al 1995 (Wolgemuth et al 1998, Buemer et al 2000, Strothmann et al 2004 Yes Androgen Binding Protein (ABP); sex hormone binding globulin…”

Section: Tablementioning

confidence: 99%

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

Meachem¹,

Ruwanpura²,

Ziolkowski³

et al. 2005

Journal of Endocrinology

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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 FSH shifts between 9 and 18 day postpartum (dpp) during the first wave of spermatogenesis from driving Sertoli cell proliferation to support germ cells. To enable comprehensive analysis of the impact of acute in vivo FSH suppression on Sertoli and germ cell development, FSH was selectively suppressed in Sprague-Dawley rats by passive immunisation for 2 days and/or 4 days prior to testis collection at 3, 9 and 18 dpp. The 3 dpp samples displayed no measurable changes, while 4 days of FSH suppression decreased Sertoli cell proliferation and numbers in 9 dpp, but not 18 dpp, animals. In contrast, germ cell numbers were unaffected at 9 dpp but decreased at 18 dpp following FSH suppression, with a corresponding increase in germ cell apoptosis measured at 18 dpp. Sixty transcripts were measured as changed at 18 dpp in response to 4 days of FSH suppression, as assessed using Affymetrix 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 differentially affects Sertoli and germ cells in an age-dependent manner in vivo, promoting Sertoli cell mitosis at day 9, and supporting germ cell viability at day 18. This model has enabled identification of candidate genes that contribute to the FSH-mediated pathway by which Sertoli cells support germ cells.

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“…Other studies have examined the acute effects of testosterone or FSH in hypogonadal (hpg) [15,16] or neonatal [17] mice. The effects of FSH also have been examined in mouse Sertoli cell lines by overexpressing a constitutively active FSH receptor [18].…”

Section: Introductionmentioning

confidence: 99%

Changes in Gene Expression in Somatic Cells of Rat Testes Resulting from Hormonal Modulation and Radiation-Induced Germ Cell Depletion1

Zhou

Bolden-Tiller

Shetty

et al. 2010

Biology of Reproduction

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Although gonadotropins and androgen are required for normal spermatogenesis and both testosterone and follicle-stimulating hormone (FSH) are responsible for the inhibition of spermatogonial differentiation that occurs in irradiated rats, it has been difficult to identify the specific genes involved. To study specific hormonally regulated changes in somatic cell gene expression in the testis that may be involved in these processes, without the complication of changing populations of germ cells, we used irradiated LBNF(1) rats, the testes of which contain almost exclusively somatic cells except for a few type A spermatogonia. Three different groups of these rats were treated with various combinations of gonadotropin-releasing hormone antagonist, an androgen receptor antagonist (flutamide), testosterone, and FSH, and we compared the gene expression levels 2 wk later to those of irradiated-only rats by microarray analysis. By dividing the gene expression patterns into three major patterns and 11 subpatterns, we successfully distinguished, in a single study, the genes that were specifically regulated by testosterone, by luteinizing hormone (LH), and by FSH from the large number of genes that were not hormonally regulated in the testis. We found that hormones produced more dramatic upregulation than downregulation of gene expression: Testosterone had the strongest upregulatory effect, LH had a modest but appreciable upregulatory effect, and FSH had a minor upregulatory effect. We also separately identified the somatic cell genes that were chronically upregulated by irradiation. Thus, the present study identified gene expression changes that may be responsible for hormonal action on somatic cells to support normal spermatogenesis and the hormone-mediated block in spermatogonial development after irradiation.

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Gene expression profiling of mouse Sertoli cell lines

Cited by 14 publications

References 46 publications

Targeted Inactivation of p12Cdk2ap1, CDK2 Associating Protein 1, Leads to Early Embryonic Lethality

Targeted Inactivation of p12Cdk2ap1, CDK2 Associating Protein 1, Leads to Early Embryonic Lethality

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

Changes in Gene Expression in Somatic Cells of Rat Testes Resulting from Hormonal Modulation and Radiation-Induced Germ Cell Depletion1

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