Figure 5.
Figure 5. The role of FBG Aα-RGD and Bβ1-42 cell-binding domains in mediating enhanced wound closure. Confluent monolayers of HFFs were treated with 30 μg/mL FBG, FBG-325, or FBG-ΔAαC either ATOW or 24 hours prior to wounding, FBG-PRE. (A) The intensity and pattern of FBG (left), FBG-325 (middle), and FBG-ΔAαC (right) assembled into matrix fibrils was visualized by indirect immunofluorescence. Scale bar represents 25 μm. (B) At 16 hours after wounding, wound closure was quantified as described in “Materials and methods.” The data are presented as the mean ± SEM; n = 3 to 5 per condition from 3 independent experiments.

The role of FBG Aα-RGD and Bβ1-42 cell-binding domains in mediating enhanced wound closure. Confluent monolayers of HFFs were treated with 30 μg/mL FBG, FBG-325, or FBG-ΔAαC either ATOW or 24 hours prior to wounding, FBG-PRE. (A) The intensity and pattern of FBG (left), FBG-325 (middle), and FBG-ΔAαC (right) assembled into matrix fibrils was visualized by indirect immunofluorescence. Scale bar represents 25 μm. (B) At 16 hours after wounding, wound closure was quantified as described in “Materials and methods.” The data are presented as the mean ± SEM; n = 3 to 5 per condition from 3 independent experiments.

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