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Progesterone accelerates the onset of capacitation in mouse sperm via T-type calcium channels
M Senuma1, S Yamano, K Nakagawa
1Department of Obstetrics and Gynecology, School of Medicine, University of Tokushima, Japan.
Abstract:
This study was undertaken to evaluate whether progesterone induces capacitation of mouse spermatozoa. When sperm were evaluated by chlortetracycline staining, addition of progesterone significantly increased the proportion of spermatozoa exhibiting the B pattern at 60 minutes of incubation, compared with that before incubation (23 +/- 6.2% vs. 13 +/- 2.9%, p < 0.01) and that in hTF medium without progesterone (23 +/- 6.2% vs. 13 +/- 4.2%, p < 0.01). If the redistribution of proteins in sperm plasma membrane such as protein binding calcium ion were defined as capacitation, it could be said that progesterone promoted capacitation of mouse sperm. This progesterone-induced capacitation was prevented by depletion of extracellular calcium ion and addition of NiCl2, a T-type calcium channel blocker, although thapsigargin, an inhibitor of Ca2+-ATPase, did not increase the number of capacitated sperm (B pattern; progesterone vs. progesterone + depletion of calcium ion, 18 +/- 3.5% vs. 8 +/- 2.5%, p < 0.05, progesterone vs. progesterone + NiCl2, 20 +/- 3.8% vs. 6 +/- 5.2%, p < 01). Furthermore, genistein, a protein tyrosine phosphorylation inhibitor, inhibited progesterone-induced capacitation (B pattern; progesterone vs. progesterone + genistein, 20 +/- 3.8% vs. 11 +/- 2.4%, p < 01). In conclusion, progesterone induces capacitation in mouse sperm and this capacitation may be associated with calcium influx and tyrosine phosphorylation.