AIMTo investigate mechanisms of tryptase-induced reduction of sperm motility and explore whether epidermal growth factor receptor (EGF-R) and protease activated receptor 2 (PAR-2)- associated pathways are involved.

METHODSFresh semen was collected from healthy donors (n = 15). Semen parameters and quality were assessed in accordance with the World Health Organization (WHO) criteria. Swim-up sperm were fixed and subjected to immunocytochemistry and immunoelectronmicroscopy with specific antibodies directed against PAR-2 and EGF-R. Protein extractions from swim-up spermatozoa were analyzed by Western blotting with antibodies for both receptors. Motility of spermatozoa was evaluated by computer-assisted semen analysis.

RESULTSImmunocytochemistry found PAR-2 and EGF-R in approximately 30% of examined human ejaculated spermatozoa. Both receptors were localized in the plasma membrane. Like tryptase, the PAR-2 synthetic agonist SLIGKV reduced sperm motility, and this effect was inhibited by application of two specific EGF-R pathway blockers (AG1478 and PD168393).

CONCLUSIONThe observed reduction of sperm motility by tryptase through the PAR-2 receptor involves EGF-R pathways.

Ejaculation ; Enzyme Inhibitors ; pharmacology ; Humans ; Male ; Microscopy, Immunoelectron ; Oligopeptides ; pharmacology ; Quinazolines ; pharmacology ; Receptor, Epidermal Growth Factor ; antagonists & inhibitors ; drug effects ; physiology ; Receptor, PAR-2 ; physiology ; Reference Values ; Semen ; physiology ; Sperm Motility ; drug effects ; physiology ; Spermatozoa ; drug effects ; physiology ; ultrastructure ; Tyrphostins ; pharmacology