title: Keloids demonstrate high-level epidermal expression of vascular endothelial growth factor.
abstract: BACKGROUND
  Keloids are a major cause of morbidity, and arise after operation, injury, or cutaneous infection. Clinically, keloids differ from hypertrophic scars in that they grow beyond the original borders of the injury. Keloids occur most commonly for patients of African and Asian descent, and treatment options are multiple, indicating that there is no entirely satisfactory treatment for keloids. Angiogenesis inhibition has been shown to be effective in treatment of malignancy in both animal models and human beings.
  
  
  OBJECTIVE
  We sought to determine whether keloids produce the potent angiogenic factor vascular endothelial growth factor (VEGF).
  
  
  METHODS
  We performed in situ hybridization for VEGF on keloid tissue and normal skin.
  
  
  RESULTS
  Our study demonstrated abundant production of VEGF in keloids and, surprisingly, the major source of VEGF was the overlying epidermis.
  
  
  CONCLUSIONS
  Our results suggest that the overlying epidermis is the major source of keloid angiogenesis. These findings demonstrate that keloids are angiogenic lesions. Topical antiangiogenic therapy, directed at either down-regulating epidermal VEGF or inhibiting keratinocyte-derived VEGF activity on its endothelial receptors, may be useful in the treatment of keloids.
authors.affiliation: Department of Dermatology, Emory University School of Medicine and Atlanta Veterans Administration Medical Center, Atlanta, Georgia 30322, USA.
authors.forename: Amy Kim
authors.initials: AK
authors.lastname: Gira
authors.forename: Lawrence F
authors.initials: LF
authors.lastname: Brown
authors.forename: Carl V
authors.initials: CV
authors.lastname: Washington
authors.forename: Cynthia
authors.initials: C
authors.lastname: Cohen
authors.forename: Jack L
authors.initials: JL
authors.lastname: Arbiser
mesh_terms: D004817:Epidermis / Q000378:metabolism*; D006801:Humans; D017403:In Situ Hybridization; D007627:Keloid / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis*
chemical_list: D042461:Vascular Endothelial Growth Factor A