Abstract
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 α IIbβ3 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.
| Lingua originale | Inglese |
|---|---|
| pagine (da-a) | 4550-4554 |
| Numero di pagine | 5 |
| Rivista | FEBS Letters |
| Volume | 579 |
| Numero di pubblicazione | 20 |
| DOI | |
| Stato di pubblicazione | Pubblicato - 15 ago 2005 |
| Pubblicato esternamente | Sì |