Estrogen, a female hormone involved in spermatogenesis

Carreau, Serge; Bouraïma-Lelong, Hélène; Delalande, Christelle

doi:10.2478/v10039-012-0005-y

Cited by 84 publications

(55 citation statements)

References 48 publications

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“…Estrogens play a key role during male reproduction including spermatogenesis (Carreau et al 2011(Carreau et al , 2012 and sperm maturation such as capacitation (Baldi et al 2009). Estrogen response is mediated through both genomic and non-genomic actions, where the genomic one involves binding to estrogen receptors ERs and nuclear transcription factors that activate the expression of target genes.…”

Section: Introductionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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Estrogens play a crucial role in spermatogenesis and estrogen receptor a knock-out male mice are infertile. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro; however this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. To date the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice (nZ24) to 17b-estradiol (E 2 ) at the concentration of 20 ng/ml either during puberty from the fourth to seventh week of age (nZ8), or continuously from birth for a period of 12 weeks (nZ8) at which age the animals from both groups were killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (CTC) assay. According to our results, in vivo exposure to increased E 2 concentrations caused premature sperm capacitation in the epididymis. The effect of E 2 , however, seems reversible because after the termination of the exposure premature epididymal sperm capacitation is decreased in animals treated during puberty. Furthermore the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E 2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E 2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.

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Section: Introductionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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“…Therefore, we have specifically analyzed the role of estrogens since mouse SPTs express aromatase cytochrome P450 (P450arom) the enzyme that transforms androgens into estrogens, and are shown to be affected by genetic inactivation of Esr2 or Cyp19A1 genes coding for estrogen receptor beta (ERb) and P450arom, respectively [45]. In agreement, both antiestrogens and aromatase inhibitors have been reported to interfere with SPT elongation [46,47].…”

Section: Introductionmentioning

confidence: 90%

Low 17beta-Estradiol Levels in Cnr1 Knock-Out Mice Affect Spermatid Chromatin Remodeling by Interfering with Chromatin Reorganization

Cacciola¹,

Chioccarelli²,

Altucci³

et al. 2013

Biology of Reproduction

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The type 1-cannabinoid receptor, CNR1, regulates differentiation of spermatids. Indeed, we have recently reported that the genetic inactivation of Cnr1 in mice influenced chromatin remodeling of spermatids, by reducing histone displacement and then sperm chromatin quality indices (chromatin condensation and DNA integrity). Herein, we have studied, at both central and testicular levels, the molecular signals potentially involved in histone displacement. In particular, investigation of the neuroendocrine axis involved in estrogen production demonstrated down-regulation of the axis supporting FSH/estrogen secretion in Cnr1-knockout male mice. Conversely, Cnr1-knockout male mice treated with 17beta-estradiol showed a weak increase of pituitary Fsh-beta subunit mRNA levels and a rescue of sperm chromatin quality indices demonstrating that estrogens, possibly in combination with FSH secretion, play an important role in regulating chromatin remodeling of spermatids.

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“…This complex process is precisely regulated by androgens, however, estrogens have also been shown to be involved [1,2]. Estrogens are formed in reaction www.fhc.viamedica.pl catalyzed by cytochrome P450 aromatase (P450arom) -an enzyme responsible for irreversible aromatization of androgens into estrogens [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

“…ERs regulate gene expression by direct interaction with estrogen-response elements (EREs) in the promoter of target genes [14]. The precise localization of ERs in male gonads remains the subject of numerous studies and topic of many debates [4]. In rat testes ERa was found to be localized in spermatocytes, round spermatids as well as in Leydig cells, while ERb -in Sertoli cells [15,16].…”

Section: Introductionmentioning

confidence: 99%

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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Estrogen, a female hormone involved in spermatogenesis

Cited by 84 publications

References 48 publications

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Low 17beta-Estradiol Levels in Cnr1 Knock-Out Mice Affect Spermatid Chromatin Remodeling by Interfering with Chromatin Reorganization

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

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