Inhibition of compensatory lung growth in endothelial nitric oxide synthase-deficient mice

Shari M. Leuwerke, Aditya K. Kaza, Curtis G. Tribble, Irving L. Kron, Victor E. Laubach

Research output: Contribution to journalArticle

66 Scopus citations

Abstract

Pneumonectomy results in rapid compensatory growth of the remaining lung and also leads to increased flow and shear stress, which are known to stimulate endothelial nitric oxide synthase (eNOS). Nitric oxide is an essential mediator of vascular endothelial growth factor-induced angiogenesis, which should necessarily occur during compensatory lung growth. Thus our hypothesis is that eNOS is critical for compensatory lung growth. To test this, left pneumonectomy was performed in eNOS-deficient mice (eNOS-/-), and compensatory growth of the right lung was characterized throughout 14 days postpneumonectomy and compared with wild-type pneumonectomy and sham controls. Compensatory lung growth was severely impaired in eNOS-/- mice, as demonstrated by significant reductions in lung weight index, lung volume index, and volume of respiratory region. Also, pneumonectomy-induced increases in alveolar surface density and cell proliferation were prevented in eNOS-/- mice, indicating that eNOS plays a role in alveolar hyperplasia. Compensatory lung growth was also impaired in wild-type mice treated with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester. Together, these results indicate that eNOS is critical for compensatory lung growth.

Original languageEnglish (US)
Pages (from-to)L1272-L1278
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume282
Issue number6 26-6
DOIs
StatePublished - Jan 1 2002
Externally publishedYes

Keywords

  • Alveolar proliferation
  • Angiogenesis
  • Pneumocytes
  • Pulmonary regeneration

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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