β2 integrins and SFKs mediate PMN recruitment to adherent platelets at the sites of vascular injury in mice. Arterial injury was performed as described in “Materials and methods,” and the vessels were examined one hour after injury. (A) Wild-type mice were pretreated with control F(ab)′2 or anti–β2-integrin F(ab)′2 prior to performing injury. The results presented are the average number of WBCs that accumulated along the vessel (mean ± SEM) in 4 control and 11 anti-integrin–treated animals. (B) Wild-type mice (n = 6) were pretreated with vehicle, PP1 (1.5 mg/kg; n = 8), or SU6656 (0.015 mg; n = 4) prior to injury. The results presented are the average number of WBCs that accumulated along the vessel (mean ± SEM). (C) Arterial injury was performed in wild-type (n = 3) or hck−/−fgr−/−lyn−/− mice (n = 3). The results presented are the average number of WBCs that accumulated along the vessel (mean ± SEM). Representative images of vessel sections taken from a wild-type mouse treated with vehicle (D), PP1 (E), or SU6656 (F) one hour after injury. Sections were stained with hematoxylin and eosin (left panels) or processed for immunohistochemical analysis with a polyclonal antibody to P-selectin (right panels; brown staining).
