Vasohibin attenuates bleomycin induced pulmonary fibrosis via inhibition of angiogenesis in mice

Pathology. 2010;42(5):457-62. doi: 10.3109/00313025.2010.493864.

Abstract

Aims: Much evidence suggests that vascular remodelling in the lung plays a crucial role in the development of pulmonary fibrosis. Therefore, anti-angiogenesis therapy may be a promising treatment for pulmonary fibrosis. Recently, a new inhibitor called vasohibin has been discovered to operate as an intrinsic and highly specific feedback inhibitor in the process of angiogenesis. However, to date, the effect of vasohibin on anti-angiogenesis of pulmonary fibrosis has not been examined.

Methods: In this study, we utilised vasohibin to test the potential of pulmonary fibrosis therapy. We examined the role of vasohibin in the pathophysiology of bleomycin-induced pneumopathy in mice by transfection of the vasohibin gene.

Results: The results demonstrated that transfection of the vasohibin gene could attenuate pulmonary fibrosis via inhibition of angiogenesis, which markedly decreased lymphocyte infiltration, cytokine secretion and fibroblast proliferation.

Conclusions: This method may be beneficial for treating lung fibrosis and may provide a novel strategy for clinical application in the future.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bleomycin / toxicity
  • Bronchoalveolar Lavage Fluid / chemistry
  • Bronchoalveolar Lavage Fluid / cytology
  • COS Cells / drug effects
  • COS Cells / metabolism
  • Cell Cycle Proteins / genetics*
  • Cell Proliferation / drug effects
  • Chlorocebus aethiops
  • Disease Models, Animal
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Genetic Therapy / methods*
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Lymphocytes / metabolism
  • Lymphocytes / pathology
  • Mice
  • Mice, Inbred C57BL
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / pathology
  • Neovascularization, Pathologic / prevention & control*
  • Pulmonary Fibrosis / chemically induced
  • Pulmonary Fibrosis / pathology
  • Pulmonary Fibrosis / therapy*
  • Transfection

Substances

  • Cell Cycle Proteins
  • Vash1 protein, mouse
  • Bleomycin