title: Transplantation of endothelial progenitor cells accelerates dermal wound healing with increased recruitment of monocytes/macrophages and neovascularization.
abstract: Endothelial progenitor cells (EPCs) act as endothelial precursors that promote new blood vessel formation and increase angiogenesis by secreting growth factors and cytokines in ischemic tissues. These facts prompt the hypothesis that EPC transplantation should accelerate the wound-repair process by facilitating neovascularization and the production of various molecules related to wound healing. In a murine dermal excisional wound model, EPC transplantation accelerated wound re-epithelialization compared with the transplantation of mature endothelial cells (ECs) in control mice. When the wounds were analyzed immunohistochemically, the EPC-transplanted group exhibited significantly more monocytes/macrophages in the wound at day 5 after injury than did the EC-transplanted group. This observation is consistent with enzyme-linked immunosorbent assay results showing that EPCs produced in abundance several chemoattractants of monocytes and macrophages that are known to play a pivotal role in the early phase of wound healing. At day 14 after injury, the EPC-transplanted group showed a statistically significant increase in vascular density in the granulation tissue relative to that of the EC-transplanted group. Fluorescence microscopy revealed that EPCs preferentially moved into the wound and were directly incorporated into newly formed capillaries in the granulation tissue. These results suggest that EPC transplantation will be useful in dermal wound repair and skin regeneration, because EPCs both promote the recruitment of monocytes/macrophages into the wound and increase neovascularization.
authors.affiliation: Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Seoul 135-710, Korea.
authors.forename: Wonhee
authors.initials: W
authors.lastname: Suh
authors.forename: Koung Li
authors.initials: KL
authors.lastname: Kim
authors.forename: Jeong-Min
authors.initials: JM
authors.lastname: Kim
authors.forename: In-Soon
authors.initials: IS
authors.lastname: Shin
authors.forename: Young-Sam
authors.initials: YS
authors.lastname: Lee
authors.forename: Jae-Young
authors.initials: JY
authors.lastname: Lee
authors.forename: Hyung-Suk
authors.initials: HS
authors.lastname: Jang
authors.forename: Jung-Sun
authors.initials: JS
authors.lastname: Lee
authors.forename: Jonghoe
authors.initials: J
authors.lastname: Byun
authors.forename: Jin-Ho
authors.initials: JH
authors.lastname: Choi
authors.forename: Eun-Seok
authors.initials: ES
authors.lastname: Jeon
authors.forename: Duk-Kyung
authors.initials: DK
authors.lastname: Kim
mesh_terms: D000818:Animals; D020405:Dermis / Q000166:cytology / Q000293:injuries; D004195:Disease Models, Animal; D004727:Endothelium / Q000166:cytology*; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000166:cytology*; D008297:Male; D051379:Mice; D008819:Mice, Nude; D009000:Monocytes / Q000166:cytology*; D018919:Neovascularization, Physiologic / Q000502:physiology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D033581:Stem Cell Transplantation; D013997:Time Factors; D014945:Wound Healing / Q000502:physiology*; D014950:Wounds, Penetrating / Q000628:therapy
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1