| Autor: |
SIERENS, JAYNE E., SNEDDON, SHARON F., COLLINS, FRANCES, MILLAR, MICHAEL R., SAUNDERS, PHILIPPA T. K. |
| Předmět: |
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| Zdroj: |
Annals of the New York Academy of Sciences; 2005, Vol. 1061 Issue 1, p65-76, 12p |
| Abstrakt: |
Levels of estrogen within the male reproductive tract are higher than in the general circulation and the aromatase enzyme is expressed in the adult testis. Estrogens such as estradiol (E2) modify cell function by binding to high-affinity estrogen receptors (ER). Two subtypes (ERα and ERβ) have been identified. Studies in animals have shown that over- or underexposure to estrogens can have an impact on testis function. For example, mice with targeted disruption of the aromatase cyp19 gene become infertile because round spermatids fail to differentiate normally. In rodents, ERα is expressed in Leydig cells; ERα mRNA and protein are not detectable in testes from humans or primates. High levels of expression of ERα occur in the efferent ductules in rodents, primates, and the human. ERβ protein has been immunolocalized to all somatic cells and to some germ cells in these same species. Messenger RNAs for splice variant isoforms of human ERβ are expressed in human testes. Homologues of the ERβ variant have been cloned from primates; this isoform does not exist in rodents and does not bind E2. Full-length ERβ protein (ERβ1) and ERβ2 have differential patterns of expression in human testes. In conclusion, although estogens are synthesized in the testis and it has been suggested that E2 may function as a germ cell survival factor, the mechanisms by which estrogens influence male fertility remain uncertain and rodents may be poor models in which to examine this. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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