These differences suggest that C15 promotes faster wound re-epithelialization, which may be directly by affecting keratinocyte migration and/or indirectly by modulating fibroblast behavior and leading to accelerated wound contraction.
In line with its role in keratinocyte migration, there is direct evidence that HB-EGF can induce EMT, enhance metastasis, and modulate chemotherapy resistance [26], [40], [41], [42].
However, in contrast, they observed a higher keratinocyte migration and proliferation in control samples.
These flexible composites provided firm attachment for keratinocytes from the outer root sheath of human hair allowing keratinocyte migration through micropores.
The capability of membranes to modulate keratinocyte differentiation inducing specific interactions in epidermal membrane systems was investigated.
KER also promotes fibroblast attachment and proliferation, keratinocyte migration, and collagen expression, which can accelerate wound healing.
Meshing or scalpel fenestration of the construct was found to stimulate keratinocyte migration and to decrease proliferation.
However, we found that GSI treatment also significantly reduced keratinocyte migration, suggesting that Notch signaling is important for keratinocyte migration and differentiation in wound healing.
These results confirmed that this inhibition of keratinocyte migration was dependent on the epitopes of the blocking antibody, and that laminin-5-β4 interareionecessarycessary for keratinocyte migration.
Interestingly, Jagged peptide treatment also significantly decreased keratinocyte migration compared to control cultures (Fig. 5c, d).
