title: Infrared exposure induces an angiogenic switch in human skin that is partially mediated by heat.
abstract: BACKGROUND
  Angiogenesis plays an important role in physiological and pathological conditions of the skin. Although acute ultraviolet-induced skin angiogenesis has been investigated, little is known about the distinct effects of acute infrared (IR) radiation on angiogenesis in human skin.
  
  
  OBJECTIVE
  To elucidate the molecular regulation of the angiogenic switch by acute near-IR radiation or by a single heat treatment in human skin in vivo.
  
  
  METHODS
  We subjected 16 healthy volunteers to near-IR irradiation (six minimal heating doses) and 14 healthy volunteers to heat treatment (43 degrees C for 90 min), and skin specimens were obtained by punch biopsy for immunohistochemical, Western blot and reverse transcription-polymerase chain reaction analyses.
  
  
  RESULTS
  We observed that CD31-stained vessels in the upper dermis were increased after acute near-IR exposure, and that this was associated with the upregulation of vascular endothelial growth factor (VEGF) and the downregulation of thrombospondin (TSP)-2. During the application of near-IR to buttock skin, skin temperatures immediately increased from 32 degrees C up to 42 degrees C, as measured using a digital thermometer. Moreover, the expression of inducible heat shock protein 70 was increased after near-IR irradiation in human skin. Therefore, we investigated the effects of a single heat treatment on angiogenesis and on the expression of VEGF and TSP-2 in skin, and found that vascularization and VEGF expression were increased, whereas TSP-2 expression was reduced.
  
  
  CONCLUSIONS
  Our results suggest that IR radiation plays an important role in skin angiogenesis via regulation of the balance between the angiogenic inducer VEGF and the angiogenic inhibitor TSP-2, and that IR-induced skin angiogenesis might be partially caused by the effects of heat in human skin in vivo.
authors.affiliation: Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul, Korea.
authors.forename: M-S
authors.initials: MS
authors.lastname: Kim
authors.forename: Y K
authors.initials: YK
authors.lastname: Kim
authors.forename: K H
authors.initials: KH
authors.lastname: Cho
authors.forename: J H
authors.initials: JH
authors.lastname: Chung
mesh_terms: D000328:Adult; D001706:Biopsy; D015152:Blotting, Northern; D015536:Down-Regulation / Q000528:radiation effects; D004817:Epidermis / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D006801:Humans; D007259:Infrared Rays / Q000009:adverse effects*; D008297:Male; D009389:Neovascularization, Pathologic / Q000209:etiology / Q000503:physiopathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000098:blood supply / Q000378:metabolism / Q000528:radiation effects*; D012881:Skin Temperature / Q000528:radiation effects; D019699:Thrombospondins / Q000096:biosynthesis*; D015854:Up-Regulation / Q000528:radiation effects; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis*; D000099262:Thrombospondin 2
chemical_list: D019699:Thrombospondins; D042461:Vascular Endothelial Growth Factor A; D000099262:Thrombospondin 2