Tanaka R, et al. - Since chronic inflammation of the dermis is one suggested reason for aberrant wound healing in keloid scars, researchers tested the assumption that the dysfunction of endothelial progenitor cells causes excessive blood vessel formation and high capillary density in keloid tissues. In keloid patients and healthy people, they compared the number of circulating endothelial progenitor cells and vasculogenic and angiogenic capacity as well as the secretory function of circulating CD34⁺ cells. Cultures of peripheral blood mononuclear cells obtained from keloid subjects exhibited a more than twofold increase in the number of peripheral blood EPCs (fibronectin-adhering cells that phagocytized acetylated low-density lipoprotein and bound Ulex europaeus agglutinin-I lectin) vs mononuclear cell cultures from healthy donors. However, there was no distinction between circulating CD34⁺ cells isolated from keloid patients and healthy people in colony-forming ability and participation in in vitro angiogenesis. This implies that normal vasculogenic and angiogenic function of CD34⁺/endothelial progenitor cells in keloid patients. CD34 + cells derived from keloid patients, however, showed more than sevenfold interleukin-8 gene expression and more than fivefold vascular endothelial growth factor gene expression than CD34⁺ cells derived from healthy people. These findings support the role of vascular endothelial growth factor and interleukin-8 in increasing endothelial progenitor cell recruitment in keloid patients.