Figure 6
Figure 6. Model for mucin-induced platelet-neutrophil interactions in Trousseau syndrome. (A) Binding of mucins to L-selectin on neutrophils and to low levels of P-selectin on resting platelets first brings these cells into closer proximity. (B) Binding of mucins and neutrophil PSGL-1 to P-selectin then activates SFKs in platelets. (C) P-selectin binding to PSGL-1 and mucin binding to L-selectin next activate SFKs in neutrophils. SFK-dependent signals in platelets and neutrophils cooperate with signaling from platelet-derived agonists to trigger cathepsin G release into the protected space between adherent neutrophils and platelets. Binding of cathepsin G to PAR4 further activates platelets to mobilize more P-selectin and cause platelet aggregation.

Model for mucin-induced platelet-neutrophil interactions in Trousseau syndrome. (A) Binding of mucins to L-selectin on neutrophils and to low levels of P-selectin on resting platelets first brings these cells into closer proximity. (B) Binding of mucins and neutrophil PSGL-1 to P-selectin then activates SFKs in platelets. (C) P-selectin binding to PSGL-1 and mucin binding to L-selectin next activate SFKs in neutrophils. SFK-dependent signals in platelets and neutrophils cooperate with signaling from platelet-derived agonists to trigger cathepsin G release into the protected space between adherent neutrophils and platelets. Binding of cathepsin G to PAR4 further activates platelets to mobilize more P-selectin and cause platelet aggregation.

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