| First Author | Ketomäki T | Year | 2019 |
| Journal | Exp Dermatol | Volume | 28 |
| Issue | 2 | Pages | 202-206 |
| PubMed ID | 30489650 | Mgi Jnum | J:302017 |
| Mgi Id | MGI:6507462 | Doi | 10.1111/exd.13851 |
| Citation | Ketomaki T, et al. (2019) R-Ras regulates vascular permeability, but not overall healing in skin wounds. Exp Dermatol 28(2):202-206 |
| abstractText | Wounds close by keratinocytes migrating from the edge of the wound and re-epithelializing the epidermis. It has been proposed that the major stimuli for wound closure are blood-derived growth factors, chemokines and cytokines. The small GTPase R-Ras, a known integrin activator, also regulates vascular permeability during angiogenesis, and blood vessels lacking R-Ras leak plasma proteins constantly. We explored whether the access to blood-derived proteins influences skin wound healing in R-Ras knockout (KO) mice. In skin wounds, R-Ras expression was mostly restricted to the vasculature in the granulation tissue. Angiogenic blood vessels in the R-Ras KO mice were significantly more permeable than in wild-type (WT) controls. Although the distances between epidermal tongues, and the panniculus carnosus muscles, were significantly longer in R-Ras KO than WT controls before the granulation tissue formation took place, there were no differences in the wound closure or re-epithelialization rates or granulation tissue formation. These findings were also corroborated in a special splint excision wound model. Our study shows that although R-Ras does not influence the skin wound healing itself, the blood vessels lacking R-Ras are leaky and thus could facilitate the access of blood-derived proteins to the wound. |
