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Introduction . Inflammation and endothelium-derived superoxides are important pathomechanisms in atherothrombotic diseases. We could previously show that the tyrosine phosphatase SHP-1 acts as a negative regulator in endothelial superoxide production. In this study we investigated the influence of SHP-1 on platelet-endothelium interaction and arterial thrombosis in TNF  α  -induced endothelial inflammation  in vivo .  Methods . Arteriolar thrombosis and platelet rolling  in vivo  were investigated in C57BL/6 mice using intravital microscopy in the dorsal skinfold chamber microcirculation model.  Results . Inhibition of SHP-1 by the specific pharmacological inhibitor sodium stibogluconate did not significantly enhance platelet-endothelium interaction  in vivo  under physiological conditions but led to an augmented fraction of rolling platelets in TNF  α  -induced systemic inflammation. Accordingly, ferric-chloride-induced arteriolar thrombus formation, which was already increased by SHP-1 inhibition, was further enhanced in the setting of TNF  α  -induced inflammation. Platelet aggregation  in vitro  as well as  ex vivo  was not influenced by SHP-1-inhibition. In cultured endothelial cells, sodium stibogluconate increased TNF  α  -induced surface expression of p-selectin and von Willebrand factor. Additionally, TNF  α   increased SHP-1 activity and protein expression.  Conclusions . The endothelial tyrosine phosphatase SHP-1 plays an important role for vascular hemostasis  in vivo,  which is crucial in TNF  α  -induced endothelial inflammation where it may serve as an autoinhibitory molecule to prevent excess inflammatory response and thrombus formation.

The Endothelial Tyrosine Phosphatase SHP-1 Plays an Important Role for Vascular Haemostasis in TNFα-Induced InflammationIn Vivo