Figure 3
Figure 3. Role of JAM-A in leukocyte responses induced by I/R injury in murine cremasteric venules as observed by IVM. (A) WT mice were given an intravenous injection of saline (control), the anti–JAM-A mAb BV-11, or an isotype-matched control mAb (both mAbs were given at a dose of 3 mg/kg); 15 minutes later, the cremaster muscle was exteriorized for observation by IVM. After taking baseline readings of leukocyte adhesion (left panel) and transmigration (right panel), the cremaster muscle was subjected to ischemia for a duration of 30 minutes followed by reperfusion, as detailed in “Materials and methods, Intravital microscopy.” Leukocyte responses of firm adhesion and transmigration were then quantified at 30-minute intervals for 120 minutes. Results are presented as means (± SEM) for n = 4-8 mice/group. (B) WT and JAM-A−/− mice were subjected to I/R injury, or were sham-operated on (as indicated), and leukocyte responses of firm adhesion (left panel) and transmigration (right panel) were quantified at 60 minutes and 120 minutes after initiation of reperfusion. The data represent means (± SEM) from n = 6 mice/group. Statistically significant differences between control and I/R groups are shown by asterisks (*P < .05, **P < .01). Additional statistical comparisons between BV-11–treated versus control mAb–treated groups and WT versus JAM-A−/− are indicated by lines and/or by number signs (#P < .05, ##P < .01).

Role of JAM-A in leukocyte responses induced by I/R injury in murine cremasteric venules as observed by IVM. (A) WT mice were given an intravenous injection of saline (control), the anti–JAM-A mAb BV-11, or an isotype-matched control mAb (both mAbs were given at a dose of 3 mg/kg); 15 minutes later, the cremaster muscle was exteriorized for observation by IVM. After taking baseline readings of leukocyte adhesion (left panel) and transmigration (right panel), the cremaster muscle was subjected to ischemia for a duration of 30 minutes followed by reperfusion, as detailed in “Materials and methods, Intravital microscopy.” Leukocyte responses of firm adhesion and transmigration were then quantified at 30-minute intervals for 120 minutes. Results are presented as means (± SEM) for n = 4-8 mice/group. (B) WT and JAM-A−/− mice were subjected to I/R injury, or were sham-operated on (as indicated), and leukocyte responses of firm adhesion (left panel) and transmigration (right panel) were quantified at 60 minutes and 120 minutes after initiation of reperfusion. The data represent means (± SEM) from n = 6 mice/group. Statistically significant differences between control and I/R groups are shown by asterisks (*P < .05, **P < .01). Additional statistical comparisons between BV-11–treated versus control mAb–treated groups and WT versus JAM-A−/− are indicated by lines and/or by number signs (#P < .05, ##P < .01).

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