Seminal vesicle protein SVS2 acts as a protectant of sperm cholesterol and regulates sperm capacitation  — ASN Events
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  3. Seminal vesicle protein SVS2 acts as a protectant of sperm cholesterol and regulates sperm capacitation 

Seminal vesicle protein SVS2 acts as a protectant of sperm cholesterol and regulates sperm capacitation  (#38)

Naoya Araki 1 , Natsuko Kawano 2 , Kenji Miyado 2 , Kaoru Yoshida 3 , Manabu Yoshida 1 4
  1. Misaki Marine Biological Station, School of Science, University of Tokyo, Miura, Kanagawa, Japan
  2. Department of Reproductive Biology, National Center for Child Health and Development, Setagaya, Tokyo, Japan
  3. Biomedial Engineering Center, Toin University of Yokohama, Yokohama, Japan
  4. Center for Marine Biology, University of Tokyo, Miura, Kanagawa, Japan

Mammalian sperm must “capacitate” to fertilize an egg 12. Contamination of seminal plasma hinders sperm capacitation, and it is thought that seminal plasma contains a “decapacitation factor” that prevents sperm capacitation 3. On the other hand, plasma membrane of the ejaculated mammalian sperm contains high levels of cholesterol, and efflux of cholesterol is required for sperm capacitation in vitro 4 . Thus, sperm capacitation in vivo is thought to be regulated by some cholesterol liberator such as albumin or high-density lipoprotein in the fluid of the female reproductive tract 5, though concentration of albumin in any places of the female reproductive tract is enough to induce capacitation.

Previously, we found that SVS2, the protein secreted from mouse seminal vesicle, acts as a decapacitation factor 6. Recently, we showed that SVS2 is indispensable for in vivo fertilization, since SVS2 protects sperm from spermicidal action of uterus 7. However, we did not examine decapaciation effect of SVS2 in vivo, since infertility of SVS2-deficient male is mainly caused by spermicidal action.

In this study, we show that SVS2 act as a protectant of cholesterol in the sperm plasma membrane; SVS2 attaches to the sperm to prevent cholesterol efflux and retrieves free cholesterol from the medium. After mating, SVS2 enters the uterus and the uterotubal junction, arresting sperm capacitation in this area. SVS2 is disappeared from the sperm in the oviductal isthmus, and there sperm capacitation occurs. Therefore, sperm capacitation in "in vivo" condition seems not to be mediated by any cholesterol liberators such as albumin, but by the cholesterol protector, SVS2; the “decapacitation factor” SVS2 plays a key role in unlocking the entopic sperm capacitation in vivo.

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  6. Kawano N, Yoshida M, Biol. Reprod. 76, 353-361, 2007.
  7. Kawano N, et al., Proc. Natl. Acad. Sci. USA 111, 4145-4150, 2014.