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Related Experiment Videos

Decrease of vascular endothelial growth factor in macrophages from long-term smokers.

K Nagai1, T Betsuyaku, Y Ito

  • 1First Dept of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.

The European Respiratory Journal
|April 2, 2005
PubMed
Summary
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Long-term smoking impairs vascular endothelial growth factor (VEGF) availability in older adults. This study found reduced VEGF in alveolar macrophages and BAL fluid of smokers, suggesting impaired angiogenesis.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Vascular endothelial growth factor (VEGF) is crucial for endothelial cell survival and angiogenesis.
  • Alveolar macrophages (AMs) are known to express VEGF.
  • The impact of smoking and aging on VEGF expression in AMs requires further investigation.

Purpose of the Study:

  • To examine the effects of long-term smoking and age on VEGF expression in AMs.
  • To investigate the expression of VEGF's receptor, fms-like tyrosine kinase (Flt)-1, in AMs.
  • To determine VEGF levels in bronchoalveolar lavage (BAL) fluid.

Main Methods:

  • Bronchoalveolar lavage (BAL) was performed on young and older volunteers with diverse smoking histories.
  • Real-time RT-PCR was used to quantify VEGF and Flt-1 mRNA in AMs.

Related Experiment Videos

  • Enzyme-linked immunosorbent assay (ELISA) measured VEGF levels in BAL fluid.
  • Main Results:

    • Older current smokers showed a 1.8-fold reduction in AM VEGF mRNA compared to nonsmokers.
    • Emphysema patients exhibited a 1.5-fold downregulation of VEGF mRNA.
    • VEGF levels in BAL fluid were significantly decreased in current smokers across all age groups.

    Conclusions:

    • Long-term smoking impairs the biological availability of VEGF in alveolar macrophages of older individuals.
    • Downregulation of VEGF isoforms (VEGF121, VEGF165) contributes to reduced VEGF mRNA.
    • While Flt-1 mRNA varied between age groups, VEGF reduction in BAL fluid suggests impaired angiogenesis in smokers.