Seminal vesicle secretion 2 acts as a protectant of sperm sterols and prevents ectopic sperm capacitation in mice.

Autor:	Araki N; Misaki Marine Biological Station, School of Science, University of Tokyo, Miura, Japan., Trencsényi G; Department of Nuclear Medicine, University of Debrecen, Debrecen, Hungary., Krasznai ZT; Department of Obstetrics and Gynecology, University of Debrecen, Debrecen, Hungary., Nizsalóczki E; Department of Biophysics and Cell Biology, University of Debrecen, Debrecen, Hungary., Sakamoto A; Misaki Marine Biological Station, School of Science, University of Tokyo, Miura, Japan., Kawano N; Department of Reproductive Biology, National Center for Child Health and Development, Tokyo, Japan., Miyado K; Department of Reproductive Biology, National Center for Child Health and Development, Tokyo, Japan., Yoshida K; Biomedical Engineering Center, Toin University of Yokohama, Yokohama, Japan., Yoshida M; Misaki Marine Biological Station, School of Science, University of Tokyo, Miura, Japan Center for Marine Biology, University of Tokyo, Miura, Japan yoshida@mmbs.s.u-tokyo.ac.jp.
Jazyk:	angličtina
Zdroj:	Biology of reproduction [Biol Reprod] 2015 Jan; Vol. 92 (1), pp. 8. Date of Electronic Publication: 2014 Nov 13.
DOI:	10.1095/biolreprod.114.120642
Abstrakt:	Seminal vesicle secretion 2 (SVS2) is a protein secreted by the mouse seminal vesicle. We previously demonstrated that SVS2 regulates fertilization in mice; SVS2 is attached to a ganglioside GM1 on the plasma membrane of the sperm head and inhibits sperm capacitation in in vitro fertilization as a decapacitation factor. Furthermore, male mice lacking SVS2 display prominently reduced fertility in vivo, which indicates that SVS2 protects spermatozoa from some spermicidal attack in the uterus. In this study, we tried to investigate the mechanisms by which SVS2 controls in vivo sperm capacitation. SVS2-deficient males that mated with wild-type partners resulted in decreased cholesterol levels on ejaculated sperm in the uterine cavity. SVS2 prevented cholesterol efflux from the sperm plasma membrane and incorporated liberated cholesterol in the sperm plasma membrane, thereby reversibly preventing the induction of sperm capacitation by bovine serum albumin and methyl-beta-cyclodextrin in vitro. SVS2 enters the uterus and the uterotubal junction, arresting sperm capacitation in this area. Therefore, our results show that SVS2 keeps sterols on the sperm plasma membrane and plays a key role in unlocking sperm capacitation in vivo. (© 2015 by the Society for the Study of Reproduction, Inc.)
Databáze:	MEDLINE
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