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Hum Reprod. 2005 Feb;20(2):456-61. Epub 2004 Dec 2.

Tryptase inhibits motility of human spermatozoa mainly by activation of the mitogen-activated protein kinase pathway.

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  • 1Department of Dermatology and Allergy, Institute for Medical Statistics and Epidemiology, Technical University Munich, Germany. weidinger@lrz.tum.de



We previously localized protease-activated receptor 2 (PAR-2) on human spermatozoa and demonstrated that activation of PAR-2 by the mast cell (MC) product tryptase inhibits sperm motility. Importantly, tryptase-secreting MCs are encountered in the male and female genital tract, implying that MC-spermatozoa interactions may be as yet unrecognized factors affecting sperm fertilizing ability. In order to elucidate how tryptase via activation of PAR-2 acts in human spermatozoa, we studied intracellular signal transduction events.


Impairment of sperm motility by tryptase was not dependent on the presence of extracellular Ca2+ and tryptase did not alter intracellular Ca2+ levels. Pre-incubation with pertussis toxin (PTX) failed to prevent tryptase effects on sperm motility. Western blot analyses revealed that tryptase increased phosphorylation of the mitogen-activated protein kinases (MAPK) ERK1/2, an effect which was blocked by the MAPK pathway inhibitor PD98059. Pre-treatment of spermatozoa with this inhibitor also blocked the inhibtion of sperm motility evoked by tryptase.


These results indicate that tryptase acts via the ERK1/2 pathway to inhibit motility of human spermatozoa.

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