Masakatsu Fujinoki1. 1. Department of Physiology, School of Medicine Dokkyo Medical University 321-0293 Mibu Tochigi Japan.
Abstract
PROPOSE: The 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). METHODS: Hamster 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. RESULTS: Progesterone-enhanced hyperactivation was significantly suppressed by the inhibitors of IP3R, PKC and PKA. CONCLUSIONS: The 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.
PROPOSE: The 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). METHODS: Hamster 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. RESULTS: Progesterone-enhanced hyperactivation was significantly suppressed by the inhibitors of IP3R, PKC and PKA. CONCLUSIONS: The 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.
Authors: Timo Strünker; Normann Goodwin; Christoph Brenker; Nachiket D Kashikar; Ingo Weyand; Reinhard Seifert; U Benjamin Kaupp Journal: Nature Date: 2011-03-17 Impact factor: 49.962
Authors: Maria E Teves; Hector A Guidobaldi; Diego R Uñates; Raul Sanchez; Werner Miska; Stephen J Publicover; Aduén A Morales Garcia; Laura C Giojalas Journal: PLoS One Date: 2009-12-08 Impact factor: 3.240