Key result
PSGL-1 deficiency in mice prolongs P-selectin retention on activated platelets versus wild-type.
Population
Mice (wild-type and PSGL-1-/-) infused with activated platelets
Comparison
PSGL-1 deficiency (PSGL-1-/- mice) vs Wild-type mice
Design
Preclinical
Authors
Loading...
May modulate platelet inflammatory signaling in preclinical models; leaves open human translational relevance.
The interaction of platelet P-selectin with PSGL-1 is crucial for endothelial activation and rapid shedding of P-selectin, which downregulates the inflammatory potential of platelets.
Dole et al. (2007) studied this question. PSGL-1 deficiency vs. Wild-type mice was evaluated on P-selectin shedding and endothelial activation. PSGL-1 deficiency in mice infused with activated platelets resulted in significantly longer retention of P-selectin on the platelet surface compared to wild-type mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: