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Keloid patients have higher peripheral blood endothelial progenitor cell counts and CD34 + cells with normal vasculogenic and angiogenic function that overexpress vascular endothelial growth factor and interleukin‐8
Author(s) -
Tanaka Rica,
Umeyama Yuri,
Hagiwara Hiroko,
ItoHirano Rie,
Fujimura Satoshi,
Mizuno Hiroshi,
Ogawa Rei
Publication year - 2019
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.14575
Subject(s) - angiogenesis , cd34 , progenitor cell , vasculogenesis , medicine , peripheral blood mononuclear cell , endothelial stem cell , keloid , vascular endothelial growth factor , endothelial progenitor cell , stem cell , pathology , immunology , cancer research , biology , microbiology and biotechnology , in vitro , biochemistry , vegf receptors
Background One suggested reason for aberrant wound healing in keloid scars is chronic inflammation of the dermis. We hypothesized that excessive blood vessel formation and high capillary density in keloid tissue is caused by dysfunction of endothelial progenitor cells. Methods We compared the number of circulating endothelial progenitor cells and vasculogenic and angiogenic capacity, as well as secretory function, of circulating CD34 + cells in keloid patients and healthy individuals. Results Compared to mononuclear cell cultures from healthy donors, cultures of peripheral blood mononuclear cells obtained from keloid patients showed 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). However, there was no difference in colony‐forming ability and participation in in vitro angiogenesis between circulating CD34 + cells isolated from keloid patients and healthy individuals. This means that circulating CD34 + /endothelial progenitor cells in keloid patients have normal vasculogenic and angiogenic function. However, CD34 + cells derived from keloid patients demonstrated a more than sevenfold expression of the interleukin‐8 gene and a more than fivefold expression of the vascular endothelial growth factor gene than CD34 + cells derived from healthy individuals. Conclusions These results support the role of vascular endothelial growth factor and interleukin‐8 in increased recruitment of endothelial progenitor cells in keloid patients.