VEGF overexpression in the astroglial cells of rat brainstem following ozone exposure

Neurotoxicology. 2008 Nov;29(6):920-7. doi: 10.1016/j.neuro.2008.09.006. Epub 2008 Sep 21.

Abstract

Ozone, a major photochemical pollutant, produces rapid damages in the pulmonary airway tract and in the central nervous system. This study focused on the neural mechanisms underlying the adaptive responses to an acute ozone exposure. Vascular endothelial growth factor (VEGF) is a factor associated with cellular recovery following brain injury. The aim of this study was to assess and localize the cellular expression of VEGF, since the central respiratory areas show a neuroplasticity in response to ozone. Adult rats were subjected to 0.5ppm ozone for 3h and then recovered for further 3h. The expression of VEGF was evaluated by immunocytochemistry in the central respiratory areas, i.e., the nucleus tractus solitarius (NTS) and the ventrolateral medulla (VLM). The data show a VEGF overexpression at the end of ozone exposure, which persisted during the 3-h recovery. Interestingly, using confocal analysis the bulk of VEGF labeling was observed in astroglial cell bodies and branches, while neuronal labeling was hardly noticed. Moreover, VEGF colocalized with IL-6 and TNFalpha in astrocytes closely apposed to blood vessel walls. The vasculature area was markedly increased (+58%) during post-ozone recovery. The data show that an acute ozone exposure affects primarily glial cells in the central nervous system. The VEGF up-regulation which persists after ozone exposure may contribute to brain repair and consecutive functional adaptations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects*
  • Astrocytes / metabolism
  • Glial Fibrillary Acidic Protein / metabolism
  • Interleukin-6 / metabolism
  • Male
  • Oxidants, Photochemical / pharmacology*
  • Ozone / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Respiratory Center / cytology*
  • Respiratory Center / drug effects
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation / drug effects*
  • Vascular Endothelial Growth Factor A / metabolism*

Substances

  • Glial Fibrillary Acidic Protein
  • Interleukin-6
  • Oxidants, Photochemical
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • Ozone