Figure 2
Figure 2. E-selectin engages PSGL-1 and CD44 through a common signaling pathway to slow neutrophil rolling. (A) Velocities of neutrophils from the indicated genotype rolling on E-selectin at the indicated site density with or without coimmobilized ICAM-1. (B) CD44−/− neutrophils or (C) PSGL-1−/− neutrophils rolling on E-selectin with or without coimmobilized ICAM-1 in the presence or absence of vehicle control DMSO, α-cyclodextrin (αCD), MβCD, or MβCD with serum. (D) CD44−/− neutrophils or (E) PSGL-1−/− neutrophils rolling on E-selectin with or without coimmobilized ICAM-1 in the presence or absence of DMSO, the Syk inhibitor piceatannol, the SFK inhibitor PP2 or its inactive analog PP3, the PI3K inhibitor LY294002, the Tec kinase inhibitor LFM-A13, or the p38 inhibitor SB203580. Except where indicated in panel A, the E-selectin density was 200 sites/μm2. The ICAM-1 density was 240 sites/μm2. The wall shear stress was 1 dyne/cm2. The data represent the mean ± SEM from 5 experiments. *P < .01.

E-selectin engages PSGL-1 and CD44 through a common signaling pathway to slow neutrophil rolling. (A) Velocities of neutrophils from the indicated genotype rolling on E-selectin at the indicated site density with or without coimmobilized ICAM-1. (B) CD44−/− neutrophils or (C) PSGL-1−/− neutrophils rolling on E-selectin with or without coimmobilized ICAM-1 in the presence or absence of vehicle control DMSO, α-cyclodextrin (αCD), MβCD, or MβCD with serum. (D) CD44−/− neutrophils or (E) PSGL-1−/− neutrophils rolling on E-selectin with or without coimmobilized ICAM-1 in the presence or absence of DMSO, the Syk inhibitor piceatannol, the SFK inhibitor PP2 or its inactive analog PP3, the PI3K inhibitor LY294002, the Tec kinase inhibitor LFM-A13, or the p38 inhibitor SB203580. Except where indicated in panel A, the E-selectin density was 200 sites/μm2. The ICAM-1 density was 240 sites/μm2. The wall shear stress was 1 dyne/cm2. The data represent the mean ± SEM from 5 experiments. *P < .01.

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