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Fig. 1 | Stem Cell Research & Therapy

Fig. 1

From: Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment

Fig. 1

Lnk deficiency improves wound repair in a murine model of an excisional wound. a Photographs of the wound were captured on days 0–10 after administration of an excisional wound to wild-type (WT) and Lnk-deficient mice. b This graph shows the proportion of the wound area at the indicated time points post wounding. Values are mean ± SEM; * p < 0.05 and ** p < 0.01 compared to the wound area in Lnk-deficient mice. c An H&E-stained section of a skin wound in WT and Lnk-deficient mice at the indicated time points post wounding. d The graph shows the proportion of the wound gap at the indicated time points post wounding. Values are mean ± SEM; ** p < 0.01 compared to the wound gap in WT mice. e Wound sites were analyzed to identify Sca-1/c-Kit-positive EPCs by FACS analysis. f Wound sites were analyzed to determine Flk-1/CD34-positive EPCs by FACS analysis. g and h The graph shows the percentage of Sca-1/c-Kit-positive cells (g) and Flk-1/CD34-positive cells (h) at wound sites of WT and Lnk-deficient mice. Values are mean ± SEM; ** p < 0.01 compared to WT mice

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Stem Cell Research & Therapy

ISSN: 1757-6512