Testosterone and oestradiol in concert protect seminiferous tubule maturation against inhibition by GnRH-antagonist

Walczak-Jędrzejowska, Renata; Kula, Krzysztof; Oszukowska, Elżbieta; Marchlewska, Katarzyna; Kula, Wojciech; Słowikowska-Hilczer, Jolanta

doi:10.1111/j.1365-2605.2011.01146.x

Cited by 10 publications

(3 citation statements)

References 48 publications

(64 reference statements)

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“…Whether the increased apoptosis in the first wave of spermatogenesis in the FSHRKO mouse has an ongoing effect on germ cell numbers in the adult FSHRKO mouse is unclear. Androgens are also reported to reduce spermatocyte apoptosis in pre-pubertal rats [19] and this is likely to explain the decline in germ cell numbers at 20d in the SCARKO mouse. At 20 days, germ cell loss was less marked in the SCARKO mouse than in the FSHRKO mouse but the effects were additive with a significantly greater effect in the FSHRKO.SCARKO mouse.…”

Section: Discussionmentioning

confidence: 95%

Testicular Development in Mice Lacking Receptors for Follicle Stimulating Hormone and Androgen

2012

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Post-natal testicular development is dependent on gonadotrophin and androgen stimulation. Follicle stimulating hormone (FSH) acts through receptors (FSHR) on the Sertoli cell to stimulate spermatogenesis while androgens promote testis growth through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells. In this study we have examined the effects on testis development of ablating FSHRs (FSHRKO mice) and/or ARs ubiquitously (ARKO mice) or specifically on the Sertoli cells (SCARKO mice). Cell numbers were measured using stereological methods. In ARKO mice Sertoli cell numbers were reduced at all ages from birth until adulthood. FSHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effects seen in the adult. Germ cell numbers were unaffected by FSHR and/or AR ablation at birth. By day 20 ubiquitous AR or FSHR ablation caused a marked reduction in germ cell numbers with a synergistic effect of losing both receptors (germ cell numbers in FSHRKO.ARKO mice were 3% of control). Germ cell numbers in SCARKO mice were less affected. By adulthood, in contrast, clear synergistic control of germ cell numbers had become established between the actions of FSH and androgen through the Sertoli cells. Leydig cell numbers were normal on day 1 and day 5 in all groups. By day 20 and in adult animals total AR or FSHR ablation significantly reduced Leydig cell numbers but Sertoli cell specific AR ablation had no effect. Results show that, prior to puberty, development of most testicular parameters is more dependent on FSH action than androgen action mediated through the Sertoli cells although androgen action through other cells types is crucial. Post-pubertally, germ cell numbers and spermatogenesis are dependent on FSH and androgen action through the Sertoli cells.

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Section: Discussionmentioning

confidence: 95%

Testicular Development in Mice Lacking Receptors for Follicle Stimulating Hormone and Androgen

2012

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“…At 20 days the first wave of spermatogenesis is ongoing and it is characterised by a marked surge in germ cell apoptosis which is necessary for subsequent normal spermatogenesis [ 56 ]. Germ cell death during the first wave is regulated by FSH [ 57 , 58 ] and, possibly, by androgen [ 59 ] and results described here show that this regulation of spermatogenesis is associated with changes in abundance of most Sertoli cell-specific transcripts.…”

Section: Discussionmentioning

confidence: 99%

Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity

et al. 2017

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BackgroundThe Sertoli cells act to induce testis differentiation and subsequent development in fetal and post-natal life which makes them key to an understanding of testis biology. As a major step towards characterisation of factors involved in Sertoli cell function we have identified Sertoli cell-specific transcripts in the mouse testis and have used the data to identify Sertoli cell-specific transcripts altered in mice lacking follicle-stimulating hormone receptors (FSHRKO) and/or androgen receptors (AR) in the Sertoli cells (SCARKO).ResultsAdult iDTR mice were injected with busulfan to ablate the germ cells and 50 days later they were treated with diphtheria toxin (DTX) to ablate the Sertoli cells. RNAseq carried out on testes from control, busulfan-treated and busulfan + DTX-treated mice identified 701 Sertoli-specific transcripts and 4302 germ cell-specific transcripts. This data was mapped against results from microarrays using testicular mRNA from 20 day-old FSHRKO, SCARKO and FSHRKO.SCARKO mice. Results show that of the 534 Sertoli cell-specific transcripts present on the gene chips, 85% were altered in the FSHRKO mice and 94% in the SCARKO mice (mostly reduced in both cases). In the FSHRKO.SCARKO mice additive or synergistic effects were seen for most transcripts. Age-dependent studies on a selected number of Sertoli cell-specific transcripts, showed that the marked effects in the FSHRKO at 20 days had largely disappeared by adulthood although synergistic effects of FSHR and AR knockout were seen.ConclusionsThese studies have identified the Sertoli cell-specific transcriptome in the mouse testis and have shown that most genes in the transcriptome are FSH- and androgen-dependent at puberty although the importance of FSH diminishes towards adulthood.Electronic supplementary materialThe online version of this article (10.1186/s12864-017-4357-3) contains supplementary material, which is available to authorized users.

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“…This pathway may account for the TP-mediated alleviation of the ENDO-induced decreases in the quantity and quality of sperm. Androgen affects seminiferous tubule growth and spermatocyte survival (Walczak-Jedrzejowska et al, 2011). However, Chandra et al (2010) showed that TP administration has no significant effects on the decrease in the serum FSH level in vanadate-treated rats.…”

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confidence: 99%

Protective effects of testosterone propionate on reproductive toxicity caused by Endosulfan in male mice

Wang

Zhou

et al. 2014

Environmental Toxicology

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To investigate the protective effect of testosterone propionate (TP) on reproductive toxicity caused by endosulfan in male mice, three group experiments were designed: the control group received 0 and 0, the endosulfan group received 0.8 and 0, and the endosulfan + TP group received 0.8 mg/kg/d endosulfan and 10 mg/kg/d TP, respectively. The results showed that TP significantly prevented the declines of concentration and motility rates in sperm, reduced the rate of sperm abnormalities in epididymis; and antagonized the decreases in spermatogenous cell and sperm numbers in testes induced by endosulfan. TP also decreased the numbers of cavities formed, prevented the decreases of plasma testosterone and androgen receptor (AR) mRNA in testicular tissue, alleviated the increase of LH induced by endosulfan. It is likely that TP relieve the reproductive toxicity by reversing the endosulfan-induced decreases in testosterone secretion and AR expression that resulted from the alteration of Leydig cell function.

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Testosterone and oestradiol in concert protect seminiferous tubule maturation against inhibition by GnRH-antagonist

Cited by 10 publications

References 48 publications

Testicular Development in Mice Lacking Receptors for Follicle Stimulating Hormone and Androgen

Testicular Development in Mice Lacking Receptors for Follicle Stimulating Hormone and Androgen

Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity

Protective effects of testosterone propionate on reproductive toxicity caused by Endosulfan in male mice

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