Figure 4.
Figure 4. Rap1a and PI3Kγ in neutrophils cooperate to mediate chemokine-triggered, but not selectin-triggered, slow rolling and chemokine-triggered arrest. (A) Rolling velocities of neutrophils of the indicated genotype on E-selectin co-immobilized with ICAM-1 and low-dose CXCL1 (0.1 μg/mL) in the presence or absence of anti-ICAM-1 mAb. (B) Percentages of neutrophils of the indicated genotype rolling, arrested and round, or arrested and spread on co-immobilized E-selectin, ICAM-1, and low-dose CXCL1. (C-F) Velocities of differentially labeled bone marrow leukocytes from mice of the indicated genotype rolling in trauma-challenged venules of cremaster muscle of WT mice, measured before and after injection of CXCL1 (50 ng) and then a blocking mAb to β2 integrins. The data represent the mean ± SEM from 5 experiments, with 5 mice in each experimental group. *P < .05 for rolling velocity; #P < .05 for percentage of rolling cells compared with that in WT, as determined by unpaired Student t test.

Rap1a and PI3Kγ in neutrophils cooperate to mediate chemokine-triggered, but not selectin-triggered, slow rolling and chemokine-triggered arrest. (A) Rolling velocities of neutrophils of the indicated genotype on E-selectin co-immobilized with ICAM-1 and low-dose CXCL1 (0.1 μg/mL) in the presence or absence of anti-ICAM-1 mAb. (B) Percentages of neutrophils of the indicated genotype rolling, arrested and round, or arrested and spread on co-immobilized E-selectin, ICAM-1, and low-dose CXCL1. (C-F) Velocities of differentially labeled bone marrow leukocytes from mice of the indicated genotype rolling in trauma-challenged venules of cremaster muscle of WT mice, measured before and after injection of CXCL1 (50 ng) and then a blocking mAb to β2 integrins. The data represent the mean ± SEM from 5 experiments, with 5 mice in each experimental group. *P < .05 for rolling velocity; #P < .05 for percentage of rolling cells compared with that in WT, as determined by unpaired Student t test.

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