title: Effects of 635nm light-emitting diode irradiation on angiogenesis in CoCl(2) -exposed HUVECs.
abstract: OBJECTIVE
  It is recognized that hypoxic/ischemic conditions leading to production of reactive oxygen species (ROS) are an important mediator of angiogenesis in the wound-healing process. Recently, low level light irradiation at 635 nm, which is used in many clinical fields, was found to decrease intracellular ROS levels, and consequently alleviate oxidative stress. The purpose of the present study was to investigate the effects of 635 nm light-emitting diode (LED) irradiation on angiogenesis in human umbilical vein endothelial cells, in an in vitro CoCl(2) -induced severe hypoxia model.
  
  
  METHODS
  The effects were assessed on cell viability, tube formation, hypoxia-inducible factor-1, vascular endothelial growth factor (VEGF), VEGF-1 and -2 protein expression, mitogen-activated protein kinase (MAPK) phosphorylation, and ROS dissociation.
  
  
  RESULTS
  The results showed that, under hypoxic/ischemic conditions, irradiation with 635 leads to reduced production and increased scavenging of intracellular ROS, which results in alleviation of VEGFR-1 suppression, enhanced VEGF expression and ERK MAPK activation, and subsequent acceleration of angiogenesis with improved cell viability and tube formation.
  
  
  CONCLUSIONS
  Taken together, irradiation with 635 nm was shown to reduce intracellular ROS production, which results in increased angiogenesis. Thus, we suggest that irradiation with 635 nm accelerate angiogenesis under hypoxic/ischemic conditions, and may prove to be a useful alternative tool in wound healing.
authors.affiliation: Department of Oral Pathology, 2nd Stage of Brain Korea 21 for School of Dentistry, Dental Science Research Institute, Chonnam National University, Bug-Gu, Gwangju, Korea.
authors.forename: Won Bong
authors.initials: WB
authors.lastname: Lim
authors.forename: Ji Sun
authors.initials: JS
authors.lastname: Kim
authors.forename: Young Jong
authors.initials: YJ
authors.lastname: Ko
authors.forename: HyukIl
authors.initials: H
authors.lastname: Kwon
authors.forename: Sang Woo
authors.initials: SW
authors.lastname: Kim
authors.forename: Heung Kee
authors.initials: HK
authors.lastname: Min
authors.forename: Oksu
authors.initials: O
authors.lastname: Kim
authors.forename: Hong Ran
authors.initials: HR
authors.lastname: Choi
authors.forename: Ok Joon
authors.initials: OJ
authors.lastname: Kim
mesh_terms: D000704:Analysis of Variance; D015153:Blotting, Western; D002470:Cell Survival; D002478:Cells, Cultured; D003035:Cobalt / Q000494:pharmacology*; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D066298:In Vitro Techniques; D054023:Lasers, Semiconductor; D018919:Neovascularization, Physiologic / Q000528:radiation effects*; D018384:Oxidative Stress / Q000528:radiation effects*; D010766:Phosphorylation; D011829:Radiation Dosage; D017382:Reactive Oxygen Species / Q000378:metabolism* / Q000528:radiation effects; D015398:Signal Transduction; D014471:Umbilical Veins / Q000166:cytology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology
chemical_list: C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D017382:Reactive Oxygen Species; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D003035:Cobalt; D040281:Vascular Endothelial Growth Factor Receptor-1; C018021:cobaltous chloride