About: In vivo exposure to 17 beta-estradiol triggers premature sperm capacitation in cauda epididymis     Goto   Sponge   NotDistinct   Permalink

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  • Estrogens play a crucial role in spermatogenesis and estrogen receptor a 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 17 beta-estradiol (E-2) 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 E-2 concentrations caused premature sperm capacitation in the epididymis. The effect of E-2, 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 E-2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E-2 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. Reproduction (2013) 145 255-263
  • Estrogens play a crucial role in spermatogenesis and estrogen receptor a 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 17 beta-estradiol (E-2) 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 E-2 concentrations caused premature sperm capacitation in the epididymis. The effect of E-2, 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 E-2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E-2 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. Reproduction (2013) 145 255-263 (en)
Title
  • In vivo exposure to 17 beta-estradiol triggers premature sperm capacitation in cauda epididymis
  • In vivo exposure to 17 beta-estradiol triggers premature sperm capacitation in cauda epididymis (en)
skos:prefLabel
  • In vivo exposure to 17 beta-estradiol triggers premature sperm capacitation in cauda epididymis
  • In vivo exposure to 17 beta-estradiol triggers premature sperm capacitation in cauda epididymis (en)
skos:notation
  • RIV/00216208:11310/13:10191736!RIV14-MSM-11310___
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • I, P(GA523/09/1793), P(GAP503/12/1834), S, Z(AV0Z50520701)
http://linked.open...iv/cisloPeriodika
  • 3
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
http://linked.open.../riv/druhVysledku
http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
http://linked.open...dnocenehoVysledku
  • 79420
http://linked.open...ai/riv/idVysledku
  • RIV/00216208:11310/13:10191736
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • activation; spermatogenesis; cd1 mice; boar sperm; testicular function; environmental estrogens; mouse spermatozoa; estrogen-receptor; camp-dependent pathway; protein-tyrosine phosphorylation (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • US - Spojené státy americké
http://linked.open...ontrolniKodProRIV
  • [E8505F83B03A]
http://linked.open...i/riv/nazevZdroje
  • Reproduction
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...vavai/riv/projekt
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 145
http://linked.open...iv/tvurceVysledku
  • Dvořáková-Hortová, Kateřina
  • Černá, Martina
  • Šebková, Nataša
  • Ded, Lukas
  • Dostalova, Pavla
  • Elzeinova, Fatima
  • Peknicova, Jana
http://linked.open...ain/vavai/riv/wos
  • 000317562900007
http://linked.open...n/vavai/riv/zamer
issn
  • 1470-1626
number of pages
http://bibframe.org/vocab/doi
  • 10.1530/REP-12-0472
http://localhost/t...ganizacniJednotka
  • 11310
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