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Met identification on human platelets: role of hepatocyte growth factor in the modulation of platelet activation
Daniela Pietrapiana1, Marilena Sala, Maria Prat
1Department of Medical Science, University A. Avogadro, Via Solaroli, 17, Novara 28100, Italy.
Circulating HGF is significantly increased in a number of thrombus-associated disorders. Since platelets play a pivotal role in thrombogenesis, the ability of HGF to interact with human platelets was investigated. This paper shows for the first time that human platelets express HGF receptor, the tyrosine kinase encoded by c-MET gene. At physiological concentrations HGF was found to inhibit both glycoprotein (alpha)IIb(beta)3 activation and thrombin-dependent platelet aggregation in a dose- and time-dependent manner. These results suggest that circulating HGF may counteract thrombogenesis by negatively modulating platelet functions.
Circulating HGF is significantly increased in a number of thrombus-associated disorders. Since platelets play a pivotal role in thrombogenesis, the ability of HGF to interact with human platelets was investigated. This paper shows for the first time that human platelets express HGF receptor, the tyrosine kinase encoded by c-MET gene. At physiological concentrations HGF was found to inhibit both glycoprotein (alpha)IIb(beta)3 activation and thrombin-dependent platelet aggregation in a dose- and time-dependent manner. These results suggest that circulating HGF may counteract thrombogenesis by negatively modulating platelet functions.
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