In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis
Jazyk angličtina Země Anglie, Velká Británie Médium electronic-print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
23319664
DOI
10.1530/rep-12-0472
PII: REP-12-0472
Knihovny.cz E-zdroje
- MeSH
- biologické markery metabolismus MeSH
- časové faktory MeSH
- chlortetracyklin metabolismus MeSH
- epididymis účinky léků metabolismus patologie MeSH
- estradiol aplikace a dávkování krev MeSH
- faktor TFF1 MeSH
- fluorescenční protilátková technika MeSH
- fosforylace MeSH
- kapacitace spermií účinky léků MeSH
- myši MeSH
- peptidy genetika metabolismus MeSH
- rozvrh dávkování léků MeSH
- sexuální vývoj MeSH
- spermie účinky léků metabolismus patologie MeSH
- testis účinky léků metabolismus patologie MeSH
- tyrosin MeSH
- věkové faktory MeSH
- western blotting MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- biologické markery MeSH
- chlortetracyklin MeSH
- estradiol MeSH
- faktor TFF1 MeSH
- peptidy MeSH
- Tff1 protein, mouse MeSH Prohlížeč
- tyrosin MeSH
Estrogens play a crucial role in spermatogenesis and estrogen receptor α knock-out male mice are infertile. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro; however this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. To date the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice (n=24) to 17β-estradiol (E2) at the concentration of 20 ng/ml either during puberty from the fourth to seventh week of age (n=8), or continuously from birth for a period of 12 weeks (n=8) at which age the animals from both groups were killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (CTC) assay. According to our results, in vivo exposure to increased E2 concentrations caused premature sperm capacitation in the epididymis. The effect of E2, however, seems reversible because after the termination of the exposure premature epididymal sperm capacitation is decreased in animals treated during puberty. Furthermore the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.
Citace poskytuje Crossref.org
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New Insight into Sperm Capacitation: A Novel Mechanism of 17β-Estradiol Signalling
