孕酮通过IP-PKC和PKA信号增强精子超激活。
Progesterone-enhanced sperm hyperactivation through IP-PKC and PKA signals.
作者信息
Fujinoki Masakatsu
机构信息
Department of Physiology, School of Medicine Dokkyo Medical University 321-0293 Mibu Tochigi Japan.
出版信息
Reprod Med Biol. 2012 Sep 12;12(1):27-33. doi: 10.1007/s12522-012-0137-6. eCollection 2013 Jan.
PROPOSE
The present study examined whether regulation of progesterone-enhanced hyperactivation of spermatozoa is associated with the production of inositol 1,4,5-trisphosphate (IP) 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 IP receptor (IPR), 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 IPR, PKC and PKA.
CONCLUSIONS
The results suggest that progesterone-enhanced sperm hyperactivation occurs through two signal pathways. One is an intracellular Ca signal through production of IP and DAG by PLC, binding of IP to IPR and activation of PKC by DAG and Ca. The other is a cAMP-PKA signal through production of cAMP by AC and activation of PKA by cAMP.
目的
本研究探讨孕酮增强精子超活化的调节是否与磷脂酶C（PLC）产生肌醇1,4,5-三磷酸（IP）和二酰基甘油（DAG）、腺苷酸环化酶（AC）产生环磷酸腺苷（cAMP）以及蛋白激酶C（PKC）和蛋白激酶A（PKA）的激活有关。
方法
将仓鼠精子在改良的台氏白蛋白乳酸丙酮酸（mTALP）培养基中孵育4小时使其超活化。为了研究IP受体（IPR）、PKC和PKA对孕酮增强超活化的影响，使用了它们的抑制剂（海绵抑素C、双吲哚马来酰亚胺1和H-89）。
结果
IPR、PKC和PKA的抑制剂显著抑制了孕酮增强的超活化。
结论
结果表明，孕酮增强的精子超活化通过两条信号通路发生。一条是细胞内Ca信号通路，通过PLC产生IP和DAG，IP与IPR结合，DAG和Ca激活PKC。另一条是cAMP-PKA信号通路，通过AC产生cAMP，cAMP激活PKA。
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