PMID: 30787984Feb 23, 2019Paper

Vascular endothelial Cdc42 deficiency delays skin wound-healing processes by increasing IL-1β and TNF-α expression

American Journal of Translational Research
Mengying XuYinghua Chen

Abstract

Angiogenesis is an important step in skin wound repair. Angiogenesis is affected by the functions of many types of cells, especially endothelial cells. Cdc42 plays a vital role in endothelial cell function and vascular development; however, the role of Cdc42 in skin microvascular permeability and skin wound healing is unclear. This study investigated the involvement of Cdc42 in skin wound-healing processes based on its known roles in angiogenesis. Full-thickness skin wounds were created on wild-type and inducible vascular-endothelial-specific Cdc42-/- mice. Cdc42 deletion in endothelium affected wound healing in following ways. Reepithelialization of wounds in Cdc42-/- mice was delayed compared with that of wounds in wild-type mice. The degree of angiogenesis of wound granulation tissue was significantly lower in Cdc42-/- mice than in wild-type mice. Infiltration of F4/80+ macrophages and the expression of MCP-1, IL-1β, and TNF-α were increased in the wound bed of Cdc42-/- mice compared with wild-type mice. These results confirm that Cdc42 in endothelium is required for angiogenesis and is an essential regulator of key skin wound-healing processes.

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