Reducing endogenous estrogens during the neonatal and juvenile periods affects reproductive tract development and sperm production in postpuberal boars

Berger, Trish; McCarthy, Maureen I.; Pearl, Christopher A.; At-Taras, Eeman; Roser, Janet F.; Conley, Alan J

doi:10.1016/j.anireprosci.2007.10.003

Cited by 34 publications

(25 citation statements)

References 40 publications

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“…The letrozole-induced increase in Sertoli cell numbers at 6.5 weeks in boars treated at 1, 3, and 5 weeks mirrors the results of a previous study in which boars were treated with letrozole continuously through 8 months of age (At-Taras et al 2006a), and when treatment was restricted to the first 3 months of life (Berger et al 2008). Just as importantly, the absence of effect in boars treated only at 1 day of age, 1 week of age only, 1 and 5 weeks of age, or between 11 and 16 weeks of age clearly defines the period during which Sertoli cell proliferation in the boar is sensitive to an aromatase inhibitor.…”

Section: Discussionsupporting

confidence: 70%

“…Previous studies in our laboratory have demonstrated that the administration of letrozole, an inhibitor of estrogen synthesis, beginning in the neonatal period promotes proliferation of Sertoli cells in boars. This results in an w25% increase in Sertoli cell number, testicular weight, and sperm production (At-Taras et al 2006a, Berger et al 2008. Mechanisms regulating this increase are not yet well understood, although existing data suggest local rather than systemic mediation (At-Taras et al 2006b).…”

Section: Introductionmentioning

confidence: 99%

“…Response to letrozole treatment during weeks 1-5 of age was investigated in the first experiment. Although endogenous estrogens are suppressed for at least 4 weeks following treatment in a mature boar (Berger et al 2008), we hypothesized that effective inhibition might be shorter in growing animals. Inhibition for 2 weeks following a single oral dose of letrozole treatment was verified (preliminary data not shown); hence, treatment every other week was the most frequent treatment used for the piglets treated between 1 and 5 weeks of age.…”

Section: Animals and Treatmentmentioning

confidence: 99%

“…Similarly, while continuous inhibition of aromatase activity led to an w25% increase in number of Sertoli cells and testicular weight in boars after sexual maturity (At-Taras et al 2006a), whether this had differential effects on the first and second wave is unknown. In our previous studies (At-Taras et al 2006a, Berger et al 2008, the effects of letrozole on Sertoli cell proliferation in the first wave could not be distinguished from the effects on the second, prepubertal wave of proliferation. Understanding the time intervals when Sertoli cells are sensitive to this treatment and when they are insensitive is critical for further studies investigating mechanism(s) by which aromatase inhibition influences Sertoli cell proliferation, postpubertal testicular size, and sperm production.…”

Section: Introductionmentioning

confidence: 99%

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Stimulation of Sertoli cell proliferation: defining the response interval to an inhibitor of estrogen synthesis in the boar

et al. 2012

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Sertoli cell proliferation occurs in two major waves after birth, one neonatally and another prepubertally, each contributing to final testicular size and sperm production. However, little is known about the regulation of either wave. We have previously shown that letrozole, an inhibitor of estrogen synthesis, increases Sertoli cell number and testicular size at sexual maturity in boars. These studies were conducted to determine whether letrozole affects the first or second proliferative wave. Boars were treated with letrozole during the first wave (treatment at 1, 3, and 5 weeks), less frequently (1 week of age only, or 1 and 5 weeks), on postnatal day 1, or during the second wave (weeks 11-16). Sertoli cells were enumerated in testes and estrogen concentrations were evaluated in serum and testes. Compared with vehicle controls, letrozole reduced estrogen in boars treated at weeks 1 and 5 or 1, 3, and 5, on postnatal day 1, or prepubertally. However, Sertoli cell numbers were increased only in boars treated at 1, 3, and 5 weeks of age. Neither perinatal (1 day old) nor prepubertal letrozole treatment affected Sertoli cell numbers. Hence, Sertoli cell proliferation was sensitive to letrozole only if letrozole was administered throughout the first wave, even though estrogen synthesis was effectively inhibited at all ages. These data indicate that the neonatal but not the prepubertal window of Sertoli cell proliferation is sensitive to an inhibitor of estrogen synthesis; this suggests that these two waves are differently regulated.

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Section: Animals and Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Stimulation of Sertoli cell proliferation: defining the response interval to an inhibitor of estrogen synthesis in the boar

et al. 2012

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“…The discovery of the crucial role of estrogen-mediated fluid resorption in efferent ducts of mice, albeit not in all species, generated awareness of estrogen-mediated events in male reproduction (Lubahn et al 1993, Hess et al 2000, Pearl et al 2007). Species differences, including diametrically opposite responses to estrogens in different species, as appears to be the case for Sertoli cell proliferation, indicate the value of expanding studies to species in multiple orders of mammals (Berger et al 2008, Cappon et al 2011.…”

Section: Introductionmentioning

confidence: 99%

Steroid regulation of early postnatal development in the corpus epididymidis of pigs

Katleba

Legacki

Conley

et al. 2015

Journal of Endocrinology

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Development of the epididymis including blood-epididymal barrier formation is not required until sperm reach the epididymis peripuberally. Regulation of this development in the early postnatal period is largely unknown. The current objectives were to evaluate potential roles of endogenous estrogen and androgen signaling during early development of the corpus epididymidis and to determine the timing of formation of the bloodepididymal barrier in the pig. Effects of endogenous steroids were evaluated using littermates treated with vehicle, an aromatase inhibitor (letrozole) to reduce endogenous estrogens, an estrogen receptor antagonist (fulvestrant) or an androgen receptor antagonist (flutamide). Phosphorylated histone 3 immunohistochemistry was used to identify proliferating epithelial cells. Lanthanum nitrate and electron microscopy were used to analyze formation of the blood barrier in the corpus epididymidis. Reducing endogenous estrogens increased the number of proliferating corpus epithelial cells at 6 and 6.5 weeks of age compared with vehicle-treated boars (P!0.01 and P!0.001 respectively). Blocking androgen receptors did not alter proliferation rate at 6.5 weeks of age. Although barrier formation was similar between 6 and 6.5 weeks of age in vehicle-treated animals, intercellular barriers increased in letrozole-treated littermates at 6.5 weeks of age. Fulvestrant treatment, which should mimic aromatase inhibition for regulation through ESR1 and ESR2 signaling but potentially stimulate endogenous estrogen signaling through the G protein-coupled estrogen receptor (GPER), had the opposite effect on aromatase inhibition. These responses in conjunction with the presence of GPER in the corpus epididymidis suggest early corpus epididymal development is regulated partially by GPER.

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Impaired reproduction in adult male, but not female, rats following juvenile treatment with the aromatase inhibitor, exemestane

Cappon

Chapin

Hurtt

et al. 2011

Birth Defects Research Part B: Developmental and Reproductive T

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There were no effects on sexual maturation in either sex or on female reproductive function. Treatment of juvenile male rats caused increased cohabitation time and decreased copulation rates; pregnancy rates and litter size were not affected in rats that mated. Decreased testis (10-15%) and epididymis (20-30%) weights, and decreased Sertoli cell numbers were noted at all doses. This indicates that exemestane can reduce Sertoli cell proliferation during maturation. The sensitive window for this effect is expected to be limited to the period of Sertoli cell proliferation, which is completed by around postnatal day 15 in rats and before puberty in humans. Treatment beginning at a later time relative to the window for Sertoli cell proliferation or for a longer duration is not expected to have additional adverse effect as the effect was not shown to be degenerative.

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Reducing endogenous estrogens during the neonatal and juvenile periods affects reproductive tract development and sperm production in postpuberal boars

Cited by 34 publications

References 40 publications

Stimulation of Sertoli cell proliferation: defining the response interval to an inhibitor of estrogen synthesis in the boar

Stimulation of Sertoli cell proliferation: defining the response interval to an inhibitor of estrogen synthesis in the boar

Steroid regulation of early postnatal development in the corpus epididymidis of pigs

Impaired reproduction in adult male, but not female, rats following juvenile treatment with the aromatase inhibitor, exemestane

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