α3β1 integrin–controlled Smad7 regulates reepithelialization during wound healing in mice
J. Clin. Invest. Louise E. Reynolds, et al. 118:965 doi:10.1172/JCI33538 [
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Figure 6Inhibition of Smad7 restores migration of
Itga3–/– keratinocytes in vitro and reepithelialization in vivo.
Analysis of scratch-wound closure in WT or
Itga3–/– keratinocyte cultures untransfected (nt) or transfected with control pool (cp) or Smad7 (s7) siRNAi (
A) or sense (s) or antisense (as) Smad7 oligonucleotides (
B). Results in
A and
B represent the relative migration (fold increase) ± SEM.
n = 30–35 data points/treatment. Single-cell migration of WT and
Itga3–/– keratinocytes on Fn in the presence (+) or absence (–) of TGF-β1 and Smad7-antisense oligonucleotides (
C). Results in
C represent relative migration to untreated WT controls. H&E-stained sections of WT (
D and
E) and
Itga3–/– (
F and
G) full-thickness wounds treated with either Smad7-sense (
D and
F) or Smad7-antisense oligonucleotides (
E and
G) at 3 days after injury. Scale bar: 750 μm. (
H) Quantitation of wound widths and neoepithelial lip lengths of WT and
Itga3–/– wounds treated with either PBS control (con), Smad7-sense, or Smad7-antisense oligonucleotides 3 days after injury. *
P < 0.009 for all experiments;
†P < 0.4. Arrows represent the edges of migrating epithelial lips.
