Reproductive system: aromatase and estrogens

Carreau, Serge; Bourguiba, Sonia; Lambard, Sophie; Galeraud-Denis, I.; Genissel, Christelle; Levallet, Jérôme

doi:10.1016/s0303-7207(02)00107-7

Cited by 107 publications

(84 citation statements)

References 61 publications

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“…These findings indicate that DUSP22 modulates STAT3-mediated signaling in testis. Estrogen is also thought to have a regulatory role in the testis, because estrogen biosynthesis occurs in testicular cells and the absence of ERa caused adverse effects on spermatogenesis and steroidogenesis (Couse et al, 2001;Carreau et al, 2002). Moreover, several chemicals that are present in the environment, designated xenoestrogens, because they have the ability to bind and activate ERa, are known to affect testicular gene expression (Safe, 2004).…”

Section: Interactions Between Era and Dusp22/lmw-dsp2mentioning

confidence: 99%

DUSP22/LMW-DSP2 regulates estrogen receptor-α-mediated signaling through dephosphorylation of Ser-118

et al. 2007

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In the previous study, we demonstrated the involvement of dual specificity phosphatase 22 (DUSP22/LMW-DSP2) in regulating the leukemia inhibitory factor/interleukin-6/ signal transducer and activator of transcription 3-mediated signaling pathway. In this study, we show b-estradiol (E2)-induced DUSP22 mRNA expression in estrogen receptor a (ERa)-positive breast cancer cells, whereas E2-induced phosphorylation and activation of ERa was suppressed by overexpression of DUSP22 but not catalytically inactive mutants. Furthermore, small-interfering RNA-mediated reduction of DUSP22 expression enhanced ERa-mediated transcription and endogenous gene expression. In fact, DUSP22 associated with ERa in vivo and both endogenous proteins interacted in ERa-positive breast cancer T47D cells. These results strongly suggest that DUSP22 acts as a negative regulator of the ERamediated signaling pathway.

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Section: Interactions Between Era and Dusp22/lmw-dsp2mentioning

confidence: 99%

DUSP22/LMW-DSP2 regulates estrogen receptor-α-mediated signaling through dephosphorylation of Ser-118

et al. 2007

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“…Generally, ERs are abundantly distributed in many tissues and organs such as the central and peripheral nervous system, skeleton, lungs, and the cardiovascular and reproductive systems of females and males [4][5][6]. Studies with ER knock-out (ERKO) mice showed that a lack of receptors leads to infertility [7] and deficient sexual behaviour in males [8].…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor alpha localization in the testes of men with normal spermatogenesis

Filipiak¹,

Suliborska²,

Walczak-Jędrzejowska³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:It is known that estrogens act on the male reproductive tract by binding to estrogen receptors (ER) a and b. However, studies on ER localization in the human testis are discordant. The aim of this study was to investigate the localization of ERa in the testes of adult men with normal spermatogenesis. Semen analysis of ten adult men revealed azoospermia. FSH, LH and testosterone serum concentrations were within normal values, and the volume of the testes was normal, hence obstructive azoospermia was suspected. The tissues from testicular surgical biopsies were fixed in Bouin's fluid and embedded in paraffin. Assessments of the seminiferous epithelium (scoring 10 to -1), the number of Leydig cells (scoring 1 to 5), the areal fraction of intertubular space (IS), measurements of seminiferous tubule diameter, and the thickness of the tubular wall, were performed on microscopic sections. Immunohistochemical staining was applied with monoclonal antibodies against ERa. The mean spermatogenesis score was 10 points; IS -30.6 ± 8.1%; seminiferous tubule diameter -193.9 ± 19.4 μm; thickness of tubular wall -7.44 ± 1.1 μm; number of Leydig cells -1.6 ± 1.1 points. Immunohistochemical staining showed the localization of ERa to be in the Sertoli and Leydig cell cytoplasm, while ERa was absent in germ cells. The results of testicular tissue analysis confirmed its normal structure and normal, full spermatogenesis. The presence of ERa in Sertoli and Leydig cells in normal human testis demonstrated in this study suggests that estrogens may affect testicular function.

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“…bones, brain, nervous, cardiovascular and reproductive systems [1][2][3]. Estrogens exert their biological role by binding to estrogen receptor (ER).…”

Section: Introductionmentioning

confidence: 99%

Xenoestrogens diethylstilbestrol and zearalenone negatively influence pubertal rat's testis.

Filipiak

Walczak-Jędrzejowska²,

Oszukowska³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:The aim of this study was to assess the impact of xenoestrogens: diethylstilbestrol (DES) and zearalenone (ZEA) on rat's pubertal testis and to compare it with the effect of natural estrogen -17β-estradiol (E). Male Wistar rats were daily, subcutaneously injected at 5 th -15 th postnatal days (p.d.) with E (1.25 or 12.5 μg) or DES (1.25 or 12.5 μg) or ZEA (4 or 40 μg) or vehicle. At 16 th p.d. testes were dissected, weighted, and paraffin embedded. Following parameters were assessed: diameter and length of seminiferous tubule, numbers of spermatogonia A+intermediate+B (A/In/B), preleptotene spermatocytes (PL), leptotene+zygotene+pachytene spermatocytes (L/Z/PA) and Sertoli cells per testis. Testes weight, seminiferous tubule diameter and length were decreased by both doses of E, DES and ZEA. DES effect was the strongest, but its influence on testis weight and seminiferous tubule length, on the contrary to E and ZEA, was not dose-dependent. Similarly, DES in both doses had the most severe negative impact on the number of germ and Sertoli cells. The negative influence of E on germ cells was less pronounced. The negative effect of ZEA was seen only after administration of the higher dose on spermatogonia number, while DES and E decreased A/In/B number more evidently. Sertoli cell number were decreased after both doses of E. ZEA40 decreased Sertoli cell number while ZEA4 had no effect. Conclusion: exposure of prepubertal male rat to DES has the strongest detrimental effect on the developing testis in comparison to E and ZEA. Both, E and DES, decreased number of germ and Sertoli cells, diminished seminiferous tubule diameter, length and testis weight. ZEA had much more weaker effect than the potent estrogens.

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Reproductive system: aromatase and estrogens

Cited by 107 publications

References 61 publications

DUSP22/LMW-DSP2 regulates estrogen receptor-α-mediated signaling through dephosphorylation of Ser-118

DUSP22/LMW-DSP2 regulates estrogen receptor-α-mediated signaling through dephosphorylation of Ser-118

Estrogen receptor alpha localization in the testes of men with normal spermatogenesis

Xenoestrogens diethylstilbestrol and zearalenone negatively influence pubertal rat's testis.

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