Figure 7.
Figure 7. Macrophage migration is dependent on the fibrinogen αMβ2-binding motif but not on factor XIII–mediated fibrin crosslinking. Mice expressing a form of fibrinogen that is unable to interact with the integrin αMβ2 display increased total leukocyte counts (A) and macrophage (B) migration in sterile peritonitis. This increased migration is not seen in mice that are unable to crosslink fibrin (FXIII−/−). (C) In vitro migration of macrophages through fibrin was examined in the presence or absence of factor XIIIa. In the absence of plasminogen, macrophages were unable to migrate through a fibrin matrix regardless of the degree of factor XIIIa-mediated crosslinking (lanes A-D). In contrast, in the presence of plasminogen, macrophages are able to migrate through fibrin regardless of the degree of factor XIIIa–mediated crosslinking (lanes E-H).

Macrophage migration is dependent on the fibrinogen αMβ2-binding motif but not on factor XIII–mediated fibrin crosslinking. Mice expressing a form of fibrinogen that is unable to interact with the integrin αMβ2 display increased total leukocyte counts (A) and macrophage (B) migration in sterile peritonitis. This increased migration is not seen in mice that are unable to crosslink fibrin (FXIII−/−). (C) In vitro migration of macrophages through fibrin was examined in the presence or absence of factor XIIIa. In the absence of plasminogen, macrophages were unable to migrate through a fibrin matrix regardless of the degree of factor XIIIa-mediated crosslinking (lanes A-D). In contrast, in the presence of plasminogen, macrophages are able to migrate through fibrin regardless of the degree of factor XIIIa–mediated crosslinking (lanes E-H).

Close Modal

or Create an Account

Close Modal
Close Modal