Maturation, proliferation and apoptosis of seminal tubule cells at puberty after administration of estradiol, follicle stimulating hormone or both

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

doi:10.1111/j.1745-7262.2008.00333.x

Cited by 21 publications

(23 citation statements)

References 20 publications

(25 reference statements)

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“…FSH is a main hormone responsible for SC proliferation [2,7], and the effect of FSH can be eliminated by simultaneous administration of FSH with high dose of estradiol benzoate in immature rats [7]. However, we have shown here that decrease in serum estradiol during first 5 PNDs by TP treatment resulted in decrease in SC number on 16 th PND.…”

Section: Discussioncontrasting

confidence: 35%

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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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Section: Discussioncontrasting

confidence: 35%

“…Consequently, in animals lacking FSH activity (FSHRKO, FSHKO mice) there was a reduction in the final number of SC [6]. The key role of FSH in setting the final size of SC population in adulthood has been attributed to stimulation of SCs proliferation rather than a survival [2,7].…”

Section: Introductionmentioning

confidence: 99%

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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“…The absolute volume of the seminiferous tubules and the total length of the seminiferous tubule was determined as described previously (Walczak-Jedrzejowska et al, 2008). The percentage of seminiferous tubule cross-sections containing a clear lumen (larger than 100 μm 2 ) and the surface area of tubular lumen were determined by scoring at least 100 subsequent tubular cross-sections.…”

Section: Morphometry and Stereometry Of Seminiferous Tubulesmentioning

confidence: 99%

“…The proliferative activity of the cells was studied by immunohistochemical labelling of proliferating cell nuclear antigen (PCNA LI) as described previously (Walczak-Jedrzejowska et al, 2008). As a negative control, sections were incubated with non-immune serum instead of the primary antibody.…”

Section: Identification Of Cell Proliferation and Degenerationmentioning

confidence: 99%

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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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The long‐term effects of FSH and triiodothyronine administration during the pubertal period on Connexin 43 expression and spermatogenesis efficiency in adult rats

et al. 2015

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Follicle-stimulating hormone (FSH) and triiodothyronine (T3) are known regulatory factors of spermatogenesis initiation. Hyperstimulation of both hormones evokes regressional changes in connexin 43 expression and the seminiferous epithelium in young rats during testicular maturation. However, separate treatments with T3 reduce Sertoli cell number, which seems to be closely connected with the maturation of connexin 43 gap junctions. FSH elevates Sertoli cell number and function, but this effect may take place regardless of the presence of connexin 43-dependent intercellular communication. The aim of the study was to evaluate the later effects of such treatments. Newborn, male Wistar rats were divided randomly into experimental groups receiving daily subcutaneous injections of either 7.5 IU/animal FSH, or 100 mg/kg b.w. T3, or both substances or the same volume of vehicle (control group) until day 15 of life. The animals were sacrificed on day 50. Morphometric analysis and immunohistochemical reactions were performed using antibodies against Vimentin, Proliferating Cell Nuclear Antigen and Connexin 43 in the testis. Sertoli cell count, efficiency of spermatogenesis, and hormonal pattern were examined. Disturbances in the connexin 43 expression reduced the number of Sertoli cells, the efficiency of spermatogenesis and impaired endocrine function of testes in adult rats treated with FSH and T3 during puberty. Stimulation with FSH alone increased Sertoli cell number, but was associated with a negative effect on cell-to-cell connexin 43-dependent communication, with a consequential reduction of spermatogenesis efficiency. J. Exp. Zool. 323A: 256-265, 2015. © 2015 Wiley Periodicals, Inc.

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Maturation, proliferation and apoptosis of seminal tubule cells at puberty after administration of estradiol, follicle stimulating hormone or both

Cited by 21 publications

References 20 publications

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

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

The long‐term effects of FSH and triiodothyronine administration during the pubertal period on Connexin 43 expression and spermatogenesis efficiency in adult rats

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