Progesterone‐enhanced sperm hyperactivation through IP3–PKC and PKA signals

Reproductive Medicine and Biology - 2013
Masakatsu Fujinoki1,2
1Department of Physiology, School of Medicine, Dokkyo Medical University, 321-0293 Mibu, Tochigi, Japan
2+81-282-872124

Tóm tắt

AbstractProposeThe present study examined whether regulation of progesterone‐enhanced hyperactivation of spermatozoa is associated with the production of inositol 1,4,5‐trisphosphate (IP3) and diacylglycerol (DAG) by phospholipase C (PLC) and cyclic adenosine monophosphate (cAMP) by adenylate cyclase (AC), as well as activation of protein kinase C (PKC) and protein kinase A (PKA).MethodsHamster spermatozoa were hyperactivated by incubation for 4 h in modified Tyrode's albumin lactate pyruvate (mTALP) medium. In order to examine the effects of IP3 receptor (IP3R), PKC and PKA on progesterone‐enhanced hyperactivation, their inhibitors (xestospongin C, bisindolylmaleimide 1 and H‐89) were used.ResultsProgesterone‐enhanced hyperactivation was significantly suppressed by the inhibitors of IP3R, PKC and PKA.ConclusionsThe results suggest that progesterone‐enhanced sperm hyperactivation occurs through two signal pathways. One is an intracellular Ca2+ signal through production of IP3 and DAG by PLC, binding of IP3 to IP3R and activation of PKC by DAG and Ca2+. The other is a cAMP–PKA signal through production of cAMP by AC and activation of PKA by cAMP.

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Reproductive Medicine and Biology

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