Woo-Sung Kwon, B.S., Yoo-Jin Park, M.S., El-Sayed A. Mohamed, Ph.D., and Myung-Geol Pang, Ph.D.
Volume 99, Issue 2, Pages 354-361, February 2013
To examine how VDAC regulates sperm function in capacitation conditions
Experimental prospective study.
Academic basic research laboratory.
Male ICR and female B6D2F1/CrljOri mice (8–12 weeks old).
Female mice were superovulated with 5 IU of pregnant mare serum gonadotrophin (PMSG) given i.p., and 5 IU of human chorionic gonadotrophin (hCG) given i.p. 48 h later. Oocytes were applied to assess fertilization and embryo development.
Main Outcome Measure(s):
Immunofluorescence Assay, Computer-Assisted Sperm Analysis, Hypo-osmotic Swelling Test, Combined Hoechst 33258/Chlortetracycline Fluorescence Assessment of Capacitation Status, Measurement of [Ca2+]i and [pH]i, Western Blotting, In Vitro Fertilization
VDAC2 was localized on the acrosomal region and principal piece, while VDAC3 was localized on the acrosomal region and midpiece. Blocking VDAC with DIDS (500μM) significantly decreased motility, viability, acrosome reaction, capacitation, tyrosine phosphorylation, fertilization, and embryo development regardless of Ca2+. However, the most severe decreases were observed in the presence (+) of DIDS and absence (-) of Ca2+, respectively. A significant decrease in [Ca2+]i concentration was observed in (-) DIDS, while [pH]i was significantly increased in (-) DIDS regardless of Ca2+. However, a significantly elevated [pH]i was observed in (+) Ca2+.
Abnormal regulation of VDACs negatively affected sperm function. Thus, VDACs may be key regulators of the fertilization ability of spermatozoa.
Read the full text at: http://www.fertstert.org/article/S0015-0282(12)02240-6/fulltext