Inhibition of miR-148b Delays Wound Closure and Promotes EndMT in a Model of Wound Healing
Dermal wounds were treated with anti-miR control or siRNA control oligonucleotides and anti-miR-148b and/or SMAD2 siRNA for 7 days. (A) Left, representative images of treated wounds at 0 and 7 days post-wound-injury; scale bar, 5 mm. Right, level of wound closure is expressed as a percentage of wound area from the initial wound area (n = 8). (B) Immunohistochemical localization of CD31 (green) and FSP-1 (red) in the wound vessels; scale bars, 25 μm (magnification 630×) (n = 8), nuclei are stained with DAPI (blue). (C) Immunohistochemical localization of CD31 and SLUG in wound vessels; scale bars, 25 μm (magnification 630×) (n = 8), nuclei are stained with DAPI (blue). (D) Quantification of CD31/FSP-1 double-positive vessels and FSP-1-positive cells and CD31/SLUG double-positive vessels in the wounds; n = 8 per each group. Values are expressed as means ± SEM. *p < 0.05; **p < 0.01 versus anti-miR control. #p < 0.05 versus anti-miR-148b. Unpaired two-tailed Student’s t test and one-way ANOVA statistical test followed by Bonferroni post-hoc analyses were applied.