Progesterone primes zona pellucida-induced activation of phospholipase A2 during acrosomal exocytosis in guinea pig spermatozoa
Autor: | Qi-Xian Shi, Shu-Qing Yu, E R S Roldan, Yicheng Ni, Chen Aijun, Yu-Ying Yuan, Wen-Ying Chen, Li-Zhen Mao |
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Rok vydání: | 2005 |
Předmět: |
Male
medicine.medical_specialty Physiology medicine.drug_class Guinea Pigs Clinical Biochemistry Biology Pertussis toxin Exocytosis Phospholipases A chemistry.chemical_compound Phospholipase A2 Internal medicine medicine Animals Enzyme Inhibitors Zona pellucida Acrosome Progesterone Protein Kinase C Zona Pellucida Protein kinase C Arachidonic Acid Cell Biology Lipid Metabolism Receptor antagonist Cyclic AMP-Dependent Protein Kinases Spermatozoa Enzyme Activation Phospholipases A2 medicine.anatomical_structure Endocrinology chemistry biology.protein Aristolochic Acids lipids (amino acids peptides and proteins) Arachidonic acid Signal Transduction |
Zdroj: | Journal of Cellular Physiology. 205:344-354 |
ISSN: | 1097-4652 0021-9541 |
Popis: | We investigated, using guinea-pig spermatozoa as a model, whether phospholipase A2 (PLA2) is involved in progesterone or zona pellucida (ZP)-stimulated acrosomal exocytosis, if progesterone enhances ZP-induced activation of PLA2, and mechanisms underlying PLA2 regulation. Spermatozoa were capacitated and labeled in low Ca2+ medium with [14C]choline chloride or [14C]arachidonic acid, washed, and then exposed to millimolar Ca2+ and progesterone and/or ZP. Each agonist stimulated decrease of phosphatidylcholine (PC) and release of arachidonic acid and lysoPC, indicative of PLA2 activation. Aristolochic acid (a PLA2 inhibitor) abrogated lipid changes and exocytosis, indicating that these lipid changes are essential for exocytosis. Exposure of spermatozoa to submaximal concentrations of both progesterone and ZP resulted in a synergistic increase of arachidonic acid and lysoPC releases, and exocytosis, suggesting that, under natural conditions, both agonists interact to bring about acrosomal exocytosis. Progesterone-induced PLA2 activation appears to be mediated by a GABA(A)-like receptor, because bicuculline (a GABA(A) receptor antagonist) blocked arachidonic acid release and exocytosis. In agreement with this, GABA mimicked progesterone actions. ZP-induced activation of PLA2 seemed to be transduced via G(i) proteins because pertussis toxin blocked arachidonic acid release and acrosomal exocytosis. PLA2 may be regulated by PKC because progesterone- or ZP-induced release of arachidonic acid was blocked by the PKC inhibitors staurosporine or chelerythrine chloride. PLA2 could also be regulated by the cAMP-PKA pathway; inclusion of the PKA inhibitor 14-22 amide or H-89 led to a reduction in arachidonic acid release or exocytosis after progesterone or ZP. Taken together, these results suggest that PLA2 plays an essential role in progesterone or ZP-stimulated exocytosis with progesterone priming ZP action. |
Databáze: | OpenAIRE |
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