Preserved tissue structure of efferent ductules in aromatase-deficient mice

Toda, Katsumi; Okada, Teruhiko; Hayashi, Yoshihiro; Saibara, Toshiji

doi:10.1677/joe-08-0257

Cited by 25 publications

(34 citation statements)

References 36 publications

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“…Treatment of rats with fulvestrant (ICI 182,780), an antiestrogen that impairs estrogen action on ESR1 and ESR2, cause morphological and functional changes in the efferent ductules similar to those seen in the Esr1 -/-mice (11), including luminal dilation and reduction of the epithelial height ( Figure 1A and B). On the other hand, treatment of rats with the aromatase inhibitor anastrozole does not seem to alter significantly the morphology of the efferent ductules ( Figure 1C and D), and aromatase knockout animals do not present a significant morphological alteration of the efferent ductules (50). Combined with the results obtained with the ESR1 knockout animals, these results indicate that the presence of a functional ESR1 is mandatory to maintain the morphology and function of the efferent ductules.…”

Section: Efferent Ductulessupporting

confidence: 52%

Estrogen receptors and function in the male reproductive system

Lazari

Lucas

Yasuhara

et al. 2009

Arq Bras Endocrinol Metab

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A substantial advance in our understanding on the estrogen signaling occurred in the last decade. Estrogens interact with two receptors, ESR1 and ESR2, also known as ERα and ERβ, respectively. ESR1 and ESR2 belong to the nuclear receptor family of transcription factors. In addition to the well established transcriptional effects, estrogens can mediate rapid signaling, triggered within seconds or minutes. These rapid effects can be mediated by ESRs or the G protein-coupled estrogen receptor GPER, also known as GPR30. The effects of estrogen on cell proliferation, differentiation and apoptosis are often mediated by growth factors. The understanding of the cross-talk between androgen, estrogen and growth factors signaling pathways is therefore essential to understand the physiopathological mechanisms of estrogen action. In this review we focused on recent discoveries about the nature of the estrogen receptors, and on the signaling and function of estrogen in the male reproductive system. Arq Bras Endocrinol Metab. 2009;53(8):923-33 Keywords Estrogens; receptors, estrogen; reproduction; male resumo Durante a última década, ocorreu um avanço substancial no conhecimento da sinalização do estrógeno. Estrógenos interagem com dois receptores, ESR1 e ESR2, também conhecidos como ERα e ERβ, respectivamente. ESR1 e ESR2 pertencem à família de receptores nucleares, que funcionam como fatores de transcrição. Além dos bem estabelecidos efeitos transcricionais, os estrógenos medeiam a sinalização rápida, desencadeada dentro de segundos ou minutos. Esses efeitos rápidos podem ser mediados por ESRs ou pelo receptor de estrógeno acoplado à proteína G, GPER, também conhecido como GPR30. Os efeitos de estrógenos sobre a proliferação celular, diferenciação e apoptose são, muitas vezes, mediados por fatores de crescimento. Portanto, a compreensão da interação entre as vias de sinalização de andrógeno, estrógeno e fatores de crescimento é essencial para entender os mecanismos fisiopatológicos envolvidos na ação estrogênica. Nesta revisão, foram abordadas descobertas recentes sobre a estrutura dos receptores, a sinalização e a função do estrógeno no sistema reprodutor masculino. Arq Bras Endocrinol Metab. 2009;53(8):923-33

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Section: Efferent Ductulessupporting

confidence: 52%

Estrogen receptors and function in the male reproductive system

Lazari

Lucas

Yasuhara

et al. 2009

Arq Bras Endocrinol Metab

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“…Although effects on the efferent ductules were noted as early as 4 days after treatment (Cho et al 2003), effects on the testis were delayed, similar to those seen in the ERaKO (Eddy et al 1996;Hess et al 1997a;Weiss et al 2008), but seminiferous tubular atrophy was heterogeneous and focal, as seen in ArKO mice Robertson et al 2001Robertson et al , 2002Toda et al 2008), and not due to fluid back-pressure. Others have also found apparent direct effects of ICI 182,780 on seminiferous epithelium (Gancarczyk et al 2004;Anahara et al 2006), including effects within 6 days of treatment (Anahara et al 2006).…”

Section: Oestrogens and The Regulation Of Spermatogenesismentioning

confidence: 57%

“…Others have shown oestrogen-dependent regulation of Leydig cell Cyp17a1 (Tong et al 2004) and Star (Houk et al 2004). Although the immunolocalization of ERa has not been consistent in the seminiferous epithelium, the ArKO-soy data clearly suggested a direct effect of oestrogen on the seminiferous epithelium in the absence of efferent ductule dysfunction (Robertson et al 2002;Toda et al 2008).…”

Section: Oestrogens and The Regulation Of Spermatogenesismentioning

confidence: 96%

Oestrogens and spermatogenesis

Carreau

Hess

2010

Phil. Trans. R. Soc. B

263

220

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The role of oestrogens in male reproductive tract physiology has for a long time been a subject of debate. The testis produces significant amounts of oestrogenic hormones, via aromatase, and oestrogen receptors (ERs)a (ESR1) and ERb (ESR2) are selectively expressed in cells of the testis as well as the epididymal epithelium, depending upon species. This review summarizes the current knowledge concerning the presence and activity of aromatase and ERs in testis and sperm and the potential roles that oestrogens may have in mammalian spermatogenesis. Data show that physiology of the male gonad is in part under the control of a balance of androgens and oestrogens, with aromatase serving as a modulator.

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“…24,25 The high concentrations of systemic androgens throughout the body are a blunt force on nearly every tissue in the male, but the unique system of estrogen synthesis in the male reproductive system creates a sequestered androgen/estrogen balance that can be focused specifically on cells expressing the requisite steroid receptors. It was surprising that the P450arom knockout mouse (AromKO) did not show histopathological results [26][27][28][29] similar to the Esr1KO mouse. 6,12 Testicular degeneration in the AromKO male began with ageing and was independent of the efferent ductule abnormalities found in the Esr1KO.…”

Section: Source Of Estrogen In the Malementioning

confidence: 99%

“…Several explanations have been proposed and some have been tested. First, ESR1 expression in the efferent ductule epithelium is constitutive and thus continues to be expressed in the absence of natural ligand 29,30 and could be activated in a ligand-independent manner. [31][32][33] It is also possible that an ever-present ESR1, in the absence of estradiol, could bind a metabolite of DHT or other steroids that are present in high concentrations in the male.…”

Section: Source Of Estrogen In the Malementioning

confidence: 99%

Disruption of estrogen receptor signaling and similar pathways in the efferent ductules and initial segment of the epididymis

Hess

2014

Spermatogenesis

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Seminiferous tubular atrophy may involve indirectly the disruption of estrogen receptor-a (ESR1) function in efferent ductules of the testis. ESR1 helps to maintain fluid resorption by the ductal epithelium and the inhibition or stimulation of this activity in rodent species will lead to fluid accumulation in the lumen. If not resolved, the abnormal buildup of fluid in the head of the epididymis and efferent ductules becomes a serious problem for the testis, as it leads to an increase in testis weight, tubular dilation and seminiferous epithelial degeneration, as well as testicular atrophy. The same sequence of pathogenesis occurs if the efferent ductule lumen becomes occluded. This review provides an introduction to the role of estrogen in the male reproductive tract but focuses on the various overlapping mechanisms that could induce efferent ductule dysfunction and fluid backpressure histopathology. Although efferent ductules are difficult to find, their inclusion in routine histological evaluations is recommended, as morphological images of these delicate tubules may be essential for understanding the mechanism of testicular injury, especially if dilations are observed in the rete testis and/or seminiferous tubules.Signature Lesion:The rete testis and efferent ductules can appear dilated, as if the lumens were greatly expanded with excess fluid or the accumulation of sperm. Because the efferent ductules resorb most of the fluid arriving from the rete testis lumen, one of two mechanisms is likely to be involved: a) reduced fluid uptake, which has been caused by the disruption in estrogen receptor signaling or associated pathways; or b) an increased rate of fluid resorption, which results in luminal occlusion. Both mechanisms can lead to a temporary increase in testicular weight, tubular dilation and atrophy of the seminiferous tubules.

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Preserved tissue structure of efferent ductules in aromatase-deficient mice

Abstract: Estrogen receptor a (Esr1) is proposed to play a critical role in the regulation of testicular fluid reabsorption at efferent ductules, and disruption of the Esr1 gene (Esr1

Cited by 25 publications

References 36 publications

Estrogen receptors and function in the male reproductive system

Estrogen receptors and function in the male reproductive system

Oestrogens and spermatogenesis

Disruption of estrogen receptor signaling and similar pathways in the efferent ductules and initial segment of the epididymis

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