Protease activated receptor 2 and epidermal growth factor receptor are involved in the regulation of human sperm motility.
- Author:
Karina ZITTA
1
;
Martin ALBRECHT
;
Stephan WEIDINGER
;
Artur MAYERHOFER
;
Frank KÖHN
Author Information
- Publication Type:Journal Article
- MeSH: 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
- From: Asian Journal of Andrology 2007;9(5):690-696
- CountryChina
- Language:English
-
Abstract:
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.
