Figure 5
The role of PI3Kδ in leukocyte emigration in cremasteric postcapillary venules in response to 3 separate time points (0 to 90 minutes, 2 to 2.5 hours, and 4 to 5 hours) of MIP-2 local administration in WT and PI3Kγ-/- mice. Mice were orally administered with 25 mg/kg PI3Kδ inhibitor IC87114 or same amount of vehicle PEG-400 prior to MIP-2 superfusion on the cremaster muscle preparation for 0 to 1.5 hours or prior to MIP-2 intrascrotal injection (1 μg in 200 μL saline) and cremaster muscle preparation at 2 to 2.5 hours or 4 to 5 hours. Leukocyte emigration was determined at the indicated time points after MIP-2 treatment in WT, PI3Kγ-/-, WT + IC87114, or PI3Kγ-/- + IC87114 mice. Each group contains at least 3 mice. *P < .05 and **P < .01, respectively, as compared with each vehicle-treated group of WT mice. τ, P < .05 as compared with IC87114-treated WT mice. δδ, P < .01 as compared with vehicle-treated PI3Kγ-/- mice. Error bars represent means plus or minus SEM.

The role of PI3Kδ in leukocyte emigration in cremasteric postcapillary venules in response to 3 separate time points (0 to 90 minutes, 2 to 2.5 hours, and 4 to 5 hours) of MIP-2 local administration in WT and PI3Kγ-/- mice. Mice were orally administered with 25 mg/kg PI3Kδ inhibitor IC87114 or same amount of vehicle PEG-400 prior to MIP-2 superfusion on the cremaster muscle preparation for 0 to 1.5 hours or prior to MIP-2 intrascrotal injection (1 μg in 200 μL saline) and cremaster muscle preparation at 2 to 2.5 hours or 4 to 5 hours. Leukocyte emigration was determined at the indicated time points after MIP-2 treatment in WT, PI3Kγ-/-, WT + IC87114, or PI3Kγ-/- + IC87114 mice. Each group contains at least 3 mice. *P < .05 and **P < .01, respectively, as compared with each vehicle-treated group of WT mice. τ, P < .05 as compared with IC87114-treated WT mice. δδ, P < .01 as compared with vehicle-treated PI3Kγ-/- mice. Error bars represent means plus or minus SEM.

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