Effects of 635nm light-emitting diode irradiation on angiogenesis in CoCl(2) -exposed HUVECs

Lasers Surg Med. 2011 Apr;43(4):344-52. doi: 10.1002/lsm.21038.

Abstract

Background and objectives: 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.

Study design/materials and 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.

Conclusion: 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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Blotting, Western
  • Cell Survival
  • Cells, Cultured
  • Cobalt / pharmacology*
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Endothelial Cells / radiation effects*
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • In Vitro Techniques
  • Lasers, Semiconductor*
  • Neovascularization, Physiologic / radiation effects*
  • Oxidative Stress / radiation effects*
  • Phosphorylation
  • Radiation Dosage
  • Reactive Oxygen Species / metabolism*
  • Reactive Oxygen Species / radiation effects
  • Signal Transduction
  • Umbilical Veins / cytology
  • Vascular Endothelial Growth Factor A / metabolism
  • Vascular Endothelial Growth Factor Receptor-1 / metabolism
  • Wound Healing / physiology

Substances

  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Reactive Oxygen Species
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Cobalt
  • Vascular Endothelial Growth Factor Receptor-1
  • cobaltous chloride