Estradiol enhances the stimulatory effect of FSH on testicular maturation and contributes to precocious initiation of spermatogenesis

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

doi:10.1016/s0303-7207(01)00415-4

Cited by 59 publications

(55 citation statements)

References 58 publications

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“…This estrogenic stimulation of seasonal testis reactivation correlates with decreased levels of pituitary and plasma LH and FSH compared with control hamsters treated with cholesterol (Pak et al 2002), implying actions of estradiol within the testis that over-ride the decreased gonadotropin drive. Moreover, Kula et al (2001) demonstrated that combined treatment of neonatal rats with both FSH and estradiol markedly enhanced the efficiency of premeiotic spermatogenesis, suggesting a synergistic effect probably at the level of the Sertoli cell.…”

Section: Androgen-estrogen Interactions In Spermatogenesis 649mentioning

confidence: 95%

“…For example, treatment of neonatal rats with estradiol benzoate in the second week of life (postnatal days 5 to 11) stimulates mitosis such that the abundance of type A spermatogonia increases as assessed at day 15 (Kula 1988). In this same experimental paradigm, estradiol benzoate treatment significantly enhanced the actions of FSH on pre-meiotic differentiation at this early stage of development resulting in increased abundance of pachytene spermatocytes (Kula et al 2001). Similar stimulatory effects of diethylstilbestrol treatment in the neonatal period on the initiation of spermatogenesis in rats have also been observed associated with small increases in circulating FSH (Atanassova et al 2000).…”

Section: Androgen-estrogen Interactions In Spermatogenesis 649mentioning

confidence: 99%

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Estrogenic induction of spermatogenesis in the hypogonadal (hpg) mouse: role of androgens

Baines

Nwagwu²,

Furneaux³

et al. 2005

Reproduction

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Testicular development is arrested in the hypogonadal (hpg) mouse due to a congenital deficiency of hypothalamic gonadotropin-releasing hormone synthesis. Previous studies have demonstrated that chronic treatment of these mice with estradiol induces testicular maturation and qualitatively normal spermatogenesis, but it is not known whether these are direct effects via estrogen receptors expressed in the testis, or indirect actions via the pituitary gland. The aim of the current studies was to determine whether the actions of estradiol require the presence of androgens. Sensitive assays revealed that chronic estradiol treatment produced time-dependent increases in pituitary FSH production but no increases in pituitary LH or testicular testosterone content could be detected. As a functional test of androgen dependence, hpg mice were treated for 70 days with estradiol plus Casodex (bicalutamide), an androgen receptor antagonist. Casodex treatment markedly attenuated both the estradiol-induced increase in testicular weight and the proliferation of the seminiferous epithelium, as revealed by morphometric analysis. However, it did not affect the estradiol-induced increase in pituitary FSH content, nor did it affect estradiolinduced increases in the weight of the seminal vesicles and epididymides. We conclude that increased FSH production is not sufficient to explain the increase in testicular development induced by estradiol in hpg mice; there is a requirement for functional androgen receptors for induction of testicular growth.

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Section: Androgen-estrogen Interactions In Spermatogenesis 649mentioning

confidence: 95%

Section: Androgen-estrogen Interactions In Spermatogenesis 649mentioning

confidence: 99%

Estrogenic induction of spermatogenesis in the hypogonadal (hpg) mouse: role of androgens

Baines

Nwagwu²,

Furneaux³

et al. 2005

Reproduction

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“…Treatment with FSH of either intact neonatal rats [4], or mouse lacking LH activity [5] evidenced increase of final number of SC. Consequently, in animals lacking FSH activity (FSHRKO, FSHKO mice) there was a reduction in the final number of SC [6].…”

Section: Introductionmentioning

confidence: 93%

Administration of testosterone inhibits initiation of seminal tubule growth and decreases Sertoli cell number in the earliest period of rat's postnatal development.

Walczak-Jędrzejowska

Słowikowska-Hilczer²,

Marchlewska³

et al. 2010

Folia Histochem Cytobiol.

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Sertoli cell (SC) number determines testes size and their capacity to produce spermatozoa. In the rat SC proliferate until 15 th postnatal day (PND). Their proliferation is stimulated by FSH and inhibited by estradiol, but the role for androgens is uncertain. In this study we analyzed the effects of testosterone administration on testes growth and SC number in relation to timing of the treatment. Male rats were injected with 2.5 mg of testosterone propionate (TP) from birth until 5 th PND and autopsied either on 6 th PND [TP1-5 (6) Control groups (C) received vehicle. In the Cs serum level of estradiol was 20-fold higher (p<0.001) and FSH was 1,7-fold higher (p<0.05) on 6 th PND than on 16 th PND, while testosterone did not change. After TP blood level of testosterone increased 2200-fold on 6 th PND (p<0.05), and 8-fold on 16 th PND. In turn, continuous TP administrations resulted on 16 th PND in the increase in testosterone serum level by 2000-times of C without influence on FSH. While the treatment from birth either during initial 5 days or continuously until 15 th day decreased testicular weight (p<0.001), tubule length (p<0.05) and SC number (p<0.001), the treatment initiated on 5 th PND had no effects. TP reduced serum estradiol level on 6 th PND by 13-fold (p<0.01), but doubled it on 16 th PND. Conclusion: Neonatal rats secrete estradiol and FSH in the amounts greatly extending those presented during further development. Testosterone inhibits testicular growth and SC number acting during first 5 neonatal days by decreasing FSH secretion, but is not effective during further development. Direct inhibitory influence of testosterone or trough its increased aromatisation to estradiol beyond neonatal period may be responsible for sustained inhibition of testes growth and SC number during infancy.

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“…Increased degeneration of spermatogonia after continuous treatment could result in the absence of factors that function to block amplification of undifferentiating spermatogonia (de Rooij et al, 1985;van Keulen and de Rooij, 1975) resulting in increased proliferation of undifferentiated type A spermatogonia and stem cells between them. An unchanged secretion of endogenous FSH and estradiol, which have been shown to stimulate spermatogonia proliferation (Kula et al, 2001;Wahlgren et al, 2008;Walczak-Jedrzejowska et al, 2007;, might participate in maintaining germ cell number and density on a normal level appropriate to the age.…”

Section: Germ Cellsmentioning

confidence: 99%

“…The initiation of spermatogenesis requires FSH, testosterone and estradiol action, (Almiron and Chemes, 1988;Kula et al, 2001;Russell et al, 1987;Walczak-Jedrzejowska et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Triiodothyronine modulates initiation of spermatogenesis in rats depending on treatment timing and blood level of the hormone

Marchlewska

Kula

Walczak-Jędrzejowska

et al. 2011

Molecular and Cellular Endocrinology

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Estradiol enhances the stimulatory effect of FSH on testicular maturation and contributes to precocious initiation of spermatogenesis

Cited by 59 publications

References 58 publications

Estrogenic induction of spermatogenesis in the hypogonadal (hpg) mouse: role of androgens

Estrogenic induction of spermatogenesis in the hypogonadal (hpg) mouse: role of androgens

Administration of testosterone inhibits initiation of seminal tubule growth and decreases Sertoli cell number in the earliest period of rat's postnatal development.

Triiodothyronine modulates initiation of spermatogenesis in rats depending on treatment timing and blood level of the hormone

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