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Hum. Reprod. Advance Access originally published online on December 2, 2004
Human Reproduction 2005 20(2):456-461; doi:10.1093/humrep/deh618
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Human Reproduction vol. 20 no. 2 © European Society of Human Reproduction and Embryology 2004; all rights reserved

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

S. Weidinger1,4, A. Mayerhofer2, L. Kunz2, M. Albrecht2, M. Sbornik1, E. Wunn1, R. Hollweck3, J. Ring1 and F.M. Kohn1

1 Department of Dermatology and Allergy, 3 Institute for Medical Statistics and Epidemiology, Technical University Munich, and 2 Department of Anatomy, University of Munich, Germany

4 To whom correspondence should be addressed at: Department of Dermatology and Allergy, Technical University Munich, Biedersteiner Str. 29, D-80802 Munich, Germany. Email: weidinger{at}lrz.tum.de

BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: These results indicate that tryptase acts via the ERK1/2 pathway to inhibit motility of human spermatozoa.

Key words: ERK1/2/human spermatozoa/mast cell/motility/PAR-2/tryptase


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