Ontogeny of androgen and estrogen receptor expression in porcine testis: Effect of reducing testicular estrogen synthesis

Ramesh, Revathi; Pearl, Christopher A.; At-Taras, Eeman; Roser, Janet F.; Berger, Trish

doi:10.1016/j.anireprosci.2006.10.025

Cited by 38 publications

(23 citation statements)

References 57 publications

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“…Interactions between estrogen or estrogen receptors and androgen receptor also occur. In this way reduced endogenous estrogen levels could affect AR as well [42]. In our study ERa-immunofluorescence was prominent in the nuclei of Leydig and myoid cells, similarly as was reported by others [1,43].…”

Section: Discussionsupporting

confidence: 73%

The immunoexpression of androgen receptor, estrogen receptors alpha and beta, vanilloid type 1 receptor and cytochrome p450 aromatase in rats testis chronically treated with letrozole, an aromatase inhibitor

Pilutin

Misiakiewicz-Has²,

Kolasa³

et al. 2014

Folia Histochem Cytobiol.

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Abstract:The function of testis is under hormonal control and any disturbance of hormonal homeostasis can lead to morphological and physiological changes. Therefore the aim of the study was to investigate the expression of androgen and estrogen receptors (AR, ERs), vanilloid receptor (TRPV1), cytochrome P450 aromatase (P450arom), as well as apoptosis of cells in testis of adult rats chronically treated with letrozole (LT), a non-steroidal aromatase inhibitor, for 6 months. The testicular tissues were fixed in Bouin's fixative and embedded in paraffin. Immunohistochemistry with monoclonal antibodies (abs) against AR, ERa, P450arom, and polyclonal abs against ERb, TRPV1, caspase-3 was applied. Long-lasting estradiol deficiency, as an effect of LT treatment, produced changes in the morphology of testis and altered the expression of the studied receptors in cells of the seminiferous tubules and rate of cell apoptosis. The immunostaining for AR was found in the nuclei of Sertoli cells and the cytoplasm of spermatogonia and spermatocytes in III-IV stages of the seminiferous epithelium cycle. The intensity of staining for P450arom was lower in the testis of LT-treated rats as compared to control animals. The immunofluorescence of ERa and ERb was observed exclusively in the nuclei of Leydig cells of LT-treated rats. There were no changes in localization of TRPV1, however, the intensity of reaction was stronger in germ cells of the seminiferous epithelium after LT treatment. The apoptosis in both groups of animals was observed within the population of spermatocytes and spermatids in II and III stages of the seminiferous epithelium cycle. In testis of LT-treated rats the immunoexpression of caspase-3 was additionally found in the germ cells in I and IV stages, and Sertoli, myoid and Leydig cells. In conclusion, our results underline the important role of letrozole treatment in the proper function of male reproductive system, and additionally demonstrate that hormonal imbalance can produce the morphological abnormalities in testis.

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Section: Discussionsupporting

confidence: 73%

The immunoexpression of androgen receptor, estrogen receptors alpha and beta, vanilloid type 1 receptor and cytochrome p450 aromatase in rats testis chronically treated with letrozole, an aromatase inhibitor

Pilutin

Misiakiewicz-Has²,

Kolasa³

et al. 2014

Folia Histochem Cytobiol.

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“…The reduced estrogen concentrations in tissues and serum of letrozole-treated boars confirmed that the lack of response during this interval was not due to a failure of the drug to inhibit estrogen synthesis, suggesting that there must be a change in the responsiveness that affects Sertoli cell proliferation itself. Whether this is due to neonatal changes in steroid receptor expression or changes in other components of the response pathway remain to be determined; both ESR1 and ESR2 are present in Sertoli cells and peritubular myoid cells (Ramesh et al 2007). Despite the inhibition of estrogen, testosterone concentrations were not significantly altered.…”

Section: Discussionmentioning

confidence: 96%

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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“…Our findings are consistent with several recent reports that Sertoli cells of the hystricognath rodent, rat, cat, boar, pig, and human express Esr1. [31][32][33][34][35][36][37][38][39][40] Although it appears difficult to reconcile, the possibilities of these conflicting results in the literature with regard to the presence of ESR1 in Sertoli cells may be due to the differences in the origin, condition, and age of the samples examined and the techniques and reagents used. In rat and human testes, the controversial results are most likely attributed to the various tissue preservations and antibodies used as well as to the origin of the tissues, which have been extensively discussed in recent studies.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, the expression of Esr1 in rat Sertoli cells is downregulated by estrogen 49 whereas ESR1 in pig Sertoli cells generally decreases with age. 32 Additionally, the expression levels of ESRs in mouse and rat Sertoli cells highly depend on cell density in vitro. 50 If the cell or tissue preservation methods are not optimal or the techniques and reagents used for detection are not sensitive enough, it is perceivable that low expression levels of Esr1 mRNA or its protein in Sertoli cells may be difficult to detect.…”

Section: Discussionmentioning

confidence: 99%

“…In several earlier reports, no ESR1 protein was detected in Sertoli cells by immunohistochemistry in bank vole, bird, rat, mouse, dog, cat, goat, boar, monkey, and human (reviewed by Carreau and Hess 7 ), whereas numerous more recent studies indicate that ESR1 is present in the Sertoli cells of multiple species including the hystricognath rodent, rat, cat, boar, pig, and human. [31][32][33][34][35][36][37][38][39][40] The expression of ESRs in Sertoli cells from rat testes has recently been studied in more detail. 31,35 The transcripts and proteins of both Esr1 and Esr2 are detected in premature and adult rat Sertoli cells.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Expression of Genomic Functional Estrogen Receptor 1 in Mouse Sertoli Cells

Lin

Zhu

et al. 2014

Reprod. Sci.

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There is no consensus whether Sertoli cells express estrogen receptor 1 (Esr1). Reverse transcription-polymerase chain reaction, Western blot, and immunofluorescence demonstrated that mouse Sertoli cell lines, TM4, MSC-1, and 15P-1, and purified primary mouse Sertoli cells (PSCs) contained Esr1 messenger RNA and proteins. Incubation of Sertoli cells with 17b-estradiol (E2) or ESR1 agonist stimulated the expression of an estrogen responsive gene Greb1, which was prevented by ESR inhibitor or ESR1 antagonist. Overexpression of Esr1 in MSC-1 enhanced E2-induced Greb1 expression, while knockdown of Esr1 by small interfering RNA in TM4 attenuated the response. Furthermore, E2-induced Greb1 expression was abolished in the PSCs isolated from Amh-Cre/Esr1-floxed mice in which Esr1 in Sertoli cells were selectively deleted. Chromatin immunoprecipitation assays indicated that E2-induced Greb1 expression in Sertoli cells was mediated by binding of ESR1 to estrogen responsive elements. In summary, ligand-dependent nuclear ESR1 was present in mouse Sertoli cells and mediates a classical genomic action of estrogens.

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Ontogeny of androgen and estrogen receptor expression in porcine testis: Effect of reducing testicular estrogen synthesis

Cited by 38 publications

References 57 publications

The immunoexpression of androgen receptor, estrogen receptors alpha and beta, vanilloid type 1 receptor and cytochrome p450 aromatase in rats testis chronically treated with letrozole, an aromatase inhibitor

The immunoexpression of androgen receptor, estrogen receptors alpha and beta, vanilloid type 1 receptor and cytochrome p450 aromatase in rats testis chronically treated with letrozole, an aromatase inhibitor

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

Expression of Genomic Functional Estrogen Receptor 1 in Mouse Sertoli Cells

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