Wound healing requires complex interactions between cells resident at the damaged site and infiltrating immune cells. As healing progresses, the growth of new blood vessels is critical to provide nutrients and oxygen. Endothelial progenitor cells (EPCs) are cells that come from the bone marrow and are key to the production of new vessels, but the signals that direct their emigration from the bone marrow are unknown. In this paper, Toshikazu Kondo and colleagues at Wakayama Medical University, in Wakayama, Japan, demonstrate that the chemokine CCL5 helps to direct the recruitment of EPCs to sites of wounding by acting on the chemokine receptor CCR5. Mice that don’t express CCR5 display delayed wound healing. These findings suggest that humans who carry mutations in CCR5 may also experience problems with wound healing, and identify the CCR5/CCL5 as a potential clinical target to promote healing.
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