Progesterone‐enhanced sperm hyperactivation through IP3–PKC and PKA signals. (12th September 2012)

• Record Type: Journal Article
• Authors: Fujinoki, Masakatsu
• Is Part Of: Reproductive medicine and biology. Volume 12:Number 1(2013)
• Page Start: 27
• Page End: 33
• Publication Date: 2012-09-12
• Subjects: Capacitation -- Hyperactivation -- Non‐genomic regulation -- Progesterone -- Spermatozoa; Reproduction -- Periodicals; Reproductive health -- Periodicals; 612.6
• DOI: 10.1007/s12522-012-0137-6
• Languages: English
• ISSNs: 1445-5781

Abstract

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 (IP3 R), 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 IP3 R, PKC and PKA. Conclusions: The results suggest that progesterone‐enhanced sperm hyperactivation occurs through two signal pathways. One is an intracellular Ca 2+ signal through production of IP3 and DAG by PLC, binding of IP3 to IP3 R and activation of PKC by DAG and Ca 2+ . The other is a cAMP–PKA signal through production of cAMP by AC and activation of PKA by cAMP.