Estrogen receptors and function in the male reproductive system

Abstract

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

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

“…12 Treatment with an aromatase inhibitor [36][37][38] also showed no effect on efferent ductule morphology, but did decrease the expression of ESR2 and GPER, while increasing androgen receptor (AR) in the rat. It also delayed the development of the head of the epididymis.…”

“…6,37,46,51,58,[67][68][69]75,80,85, Deletion of Esr1 gene caused male infertility, not only due to a disruption in male sexual behavior, 31 but also because the sperm failed to mature properly in the male reproductive tract. 117,118 Treatment with ICI induced subfertility at first, but over time complete infertility 88,89 and resulted in numerous histopathological changes that were similar to those found in testes, efferent ductules and epididymides of the Esr1KO.…”

“…There was a 52% reduction in epithelial height, decreases in the endocytic apparatus, a dramatic reduction in the number and size of microvilli and also cilia. 6,29,37,47,[74][75][76]89,90,122 Thus, both direct effects (those regulating proteins necessary for ions and water fluxes) and indirect (epithelial morphology) were mediated by ESR1 inactivation in this critical region of the male tract.…”

The coagulating gland in the male greater cane rat (Thryonomys swinderianus): morphological and immunohistochemical features

“…Besides androgen, oestrogen has also been reported to play significant roles in the accessory sex glands [11,19,24]. According to Ellem and Risbridger [14] although some rapid non-genomic oestrogen signalling are now being identified, the effect of oestrogen on the accessory gland particularly the prostate gland, under normal and prostatic disease conditions are principally mediated via the two oestrogen receptors (ERa and b).…”

Analysis of Immunoexpression of Estrogen Receptor Beta and Extracellular Matrix Metalloproteinase Inducer (Emmprin) on Testicular Seminomas Nonrecurrence and Recurrence

“…15 Mekanisme terjadinya seminoma rekurensi yaitu adanya gangguan pada inhibin inhibitor yang berfungsi menghambat produksi hormon estrogen yang menyebabkan sel leydig dan sel sertoli mensekresi hormon estrogen secara berlebihan dan kemudian diikat oleh estrogen reseptor beta. Gangguan pada inhibin inhibitor pada seminoma testis disebabkan adanya kerusakan dan mutasi DNA sehingga dapat mengubah ekspresi gen. 23 Pada penelitian ini akan …”