Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our recent discovery that testicular germ cells and epididymal sperm contain active P450 aromatase suggests that the reproductive tract may be a target for estrogen. Therefore, the objective of this study was to determine if estrogen receptors (ER) are present in the avian epididymis using immunocytochemistry, northern blot analysis, and in situ hybridization. Immunoperoxidase staining for ER was found principally in nuclei of nonciliated epithelial cells of proximal and distal efferent ductules and the epididymis duct. The ciliated cells also appeared to be slightly positive in the efferent ductules. Week immunostaining was also observed in the connective tissue of the epididymis duct. Immunostaining was more intense in epithelial cells of the efferent ductules than in epithelial cells of the epididymal duct of connective tissue cells. Strong specific hybridization signals for ER mRNA corresponded to the same areas exhibiting immunocytochemical localization. The presence of ER mRNA in the epididymis was confirmed by northern blot analysis, which showed a single band corresponding to approximately 7.8 kb, similar to that found in chicken oviduct. Based on these data, we suggest that the efferent ducts of the rooster are a primary target for estrogen and that estrogen may have a role in the regulation of avian epididymal function.
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PMID:Estrogen receptors are present in the epididymis of the rooster. 928 50

The role of estrogens in the development and physiology of the male reproductive tract remains provocative, with a growing body of evidence suggesting that estrogens are able to influence normal testis development and physiology, through their classical receptors, estrogen receptor (ER)-alpha and ER-beta. We describe the identification and characterization of a new promoter that is involved in the expression of ER-alpha in the epididymis and in testis. This promoter lies on chromosome 6q25.1, approximately 16 kb upstream of the first coding exon of ER-alpha. Sequence analysis indicates that this promoter has a conventional TATA box and GC box but no upstream CAAT sequence. Alternative splicing results in at least two species of mRNA encoding ER-alpha being synthesized from this promoter. Transcription profiling of human tissues shows that, among those tested, this promoter is predominantly active only in testis and epididymal tissues. Transient transfection assays using this new promoter in a number of cell lines indicate that the region we have identified functions as a promoter and that tissue-specific regulation is likely to be dependent on inhibitory sequences greater than 1 kb upstream of the transcription start site.
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PMID:A novel promoter is involved in the expression of estrogen receptor alpha in human testis and epididymis. 1219 52

Both testosterone and its nonaromatizable metabolite dihydrotestosterone (DHT) induce spermatogenesis in gonadotropin-deficient hpg mice. Surprisingly, because aromatization is not required, estradiol (E2) also induces spermatogenesis and increases circulating FSH in hpg mice, but the mechanism remains unclear. We studied E2-induced spermatogenesis in hpg mice on an estrogen receptor (ER)-alpha (hpg/alphaERKO) or ERbeta (hpg/betaERKO) knockout or wild-type ER (hpg/WT) background treated with subdermal E2 or DHT implants for 6 wk. In hpg/WT and hpg/betaERKO, but not hpg/alphaERKO mice, E2 increased testis and epididymal weight, whereas DHT-induced increases were unaffected by ERalpha or ERbeta inactivation. E2 but not DHT treatment increased serum FSH (but not LH) in hpg/WT and hpg/betaERKO but not hpg/alphaERKO hpg mice. DHT or E2 alone increased (premeiotic) spermatogonia and (meiotic) spermatocytes without significant change in Sertoli cell numbers. DHT alone increased postmeiotic spermatids, regardless of ER presence, compared with variable ERalpha-dependent E2 postmeiotic responses. An ERalpha-mediated effect was confirmed by treating hpg mice for 6 wk by subdermal selective ER-alpha (16alpha-LE(2)) or ERbeta (8beta-VE(2)) agonist implants. ERalpha (but not ERbeta) agonist increased testis and epididymal weight, Sertoli cell, spermatogonia, meiotic, and postmeiotic germ cell numbers. Only ERalpha agonist markedly increased serum FSH, whereas either agonist induced small rises in serum LH. Administration of ERalpha agonist or E2 in the presence of functional ERalpha induced prominent gene expression of specific Sertoli (Eppin, Rhox5) and Leydig cell (Cyp11a1, Hsd3b1) markers. We conclude that E2-induced spermatogenesis in hpg mice involves an ERalpha-dependent neuroendocrine mechanism increasing blood FSH and Sertoli cell function.
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PMID:Estradiol induction of spermatogenesis is mediated via an estrogen receptor-{alpha} mechanism involving neuroendocrine activation of follicle-stimulating hormone secretion. 2041 Jan 97