Figure 1.

Skin Wound Healing Is Accelerated with C15 Treatment through Direct and Indirect Mechanisms

Four 4 mm excisional wounds were made to the dorsal skin of Sv129Ev mice. Vehicle or C15 (100 pg/wound) in 30% Pluronic gel was administered directly into the wound immediately after wounding.

(A) Schematic diagrams illustrating the location of skin wounds and measurements derived from histological sections.

(B) Immunohistochemical staining during the wound repair time course revealed increases in the number of cells expressing chemerin and ChemR23 after wounding, particularly in granulation tissue.

(C) Macroscopic photos of vehicle- and C15-treated wounds 0–14 days after wounding.

(D) Wound area relative to initial wound area at days 1, 4, and 7 after wounding.

(E) Granulation tissue area at wound midpoints.

(F) Scab loss 7 days after wounding.

(G) Representative photos of sections from day 4 wound midpoints stained with haematoxylin and eosin.

(H) Re-epithelialization quantified by measurement of the length of wound epithelial gaps and tongues on days 1, 4, and 7 after wounding.

(I) αSMA myofibroblasts in day 4 wounds.

(J) HaCaTs (human keratinocytes) were allowed to migrate for 15 hr to fill in a “scratch wound” in vitro in the presence of C15 (1–1,000 pM) or media control.

(K) Murine dermal fibroblasts were suspended in a collagen I and media mixture supplemented with 10–1,000 pM C15 or vehicle (media) control. Gels were allowed to solidify at 37°C, and gel contraction was assessed 24 and 48 hr later.

Data are expressed as means ± SEM; there were six to ten mice (D and F) or four to eight wounds (B, E, H, and I) per treatment group or four independent experiments (J and K). ^∗p < 0.05, ^∗∗p < 0.01, and ^∗∗∗p < 0.001 relative to vehicle-treated controls. See also Figure S1. The following abbreviation is used: FOV, field of view.