Suppression of progesterone-enhanced hyperactivation in hamster spermatozoa by estrogen

Abstract

In this study, I examined whether sperm hyperactivation in hamster is regulated by steroid hormones such as estrogen (estradiol, E2) and progesterone. Although sperm hyperactivation was enhanced by progesterone, 17β-estradiol (17βE2) itself did not affect sperm hyperactivation. However, 17βE2suppressed progesterone-enhanced hyperactivation in a concentration-dependent manner through non-genomic pathways when spermatozoa were exposed to 17βE2at the same time or before exposure to progesterone. When spermatozoa were exposed to 17βE2after exposure to progesterone, 17βE2did not suppress progesterone-enhanced hyperactivation. Moreover, 17α-estradiol, an inactive isomer of E2, did not suppress progesterone-enhanced hyperactivation. Observations using a FITC-conjugated 17βE2showed that it binds to the acrosome region of the sperm head. Binding of 17βE2to spermatozoa was not inhibited by progesterone, although 17βE2did not suppress progesterone-enhanced hyperactivation when spermatozoa were exposed to 17βE2after exposure to progesterone. On the other hand, binding of progesterone to spermatozoa was also not inhibited by 17βE2even if progesterone-enhanced hyperactivation was suppressed by 17βE2. Although tyrosine phosphorylations of sperm proteins were enhanced by progesterone, enhancement of tyrosine phosphorylations by progesterone was suppressed by 17βE2. Moreover, tyrosine phosphorylations were inhibited by 17βE2when only 17βE2was added to the medium. From these results, it is likely that 17βE2competitively suppresses progesterone-enhanced hyperactivation through the inhibition of tyrosine phosphorylations via non-genomic pathways.