Figure 3
Figure 3. Mechanisms regulating plg accumulation in wounds after burn wounding. (A) Comparison of the plg levels in the wound sites in the control and fibrinogen-depleted mice 24 hours after the IV injection of plg (n = 5). (B) Comparison of the plg levels in the wound sites in the control and macrophage-depleted mice 24 hours after the IV injection of plg (n ≥ 4). (C) Comparison of the plg levels in the wound sites in the control and neutrophil-depleted mice 24 hours after the IV injection of plg (n ≥ 6). (D) Comparison of the plg or BSA accumulation in the wounded areas in the plg-injected (n = 12) and BSA-injected mice (n = 6). The level of plg or BSA in the abdominal skin was used as the basal level. The level of plg or BSA in the wound was determined and is displayed as the fold increase from the basal level. ns indicates not significant. *P < .05; **P < .01.

Mechanisms regulating plg accumulation in wounds after burn wounding. (A) Comparison of the plg levels in the wound sites in the control and fibrinogen-depleted mice 24 hours after the IV injection of plg (n = 5). (B) Comparison of the plg levels in the wound sites in the control and macrophage-depleted mice 24 hours after the IV injection of plg (n ≥ 4). (C) Comparison of the plg levels in the wound sites in the control and neutrophil-depleted mice 24 hours after the IV injection of plg (n ≥ 6). (D) Comparison of the plg or BSA accumulation in the wounded areas in the plg-injected (n = 12) and BSA-injected mice (n = 6). The level of plg or BSA in the abdominal skin was used as the basal level. The level of plg or BSA in the wound was determined and is displayed as the fold increase from the basal level. ns indicates not significant. *P < .05; **P < .01.

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