Endothelin-1 induces bronchial myofibroblast differentiation

Peptides. 1997;18(9):1449-51. doi: 10.1016/s0196-9781(97)00194-0.

Abstract

Endothelin-1 may contribute to bronchial smooth muscle constriction and airway remodelling in asthma, where bronchial epithelial cells represent an important source of this peptide. We report here that asthmatic bronchial epithelial cells exposed to allergens in vitro induce the differentiation of airway fibroblasts into myofibroblasts, and that they do so through a granulocyte/macrophage colony-stimulating factor-mediated upregulation of endothelin-1 production. By this mechanism bronchial epithelial cells may participate in the genesis of bronchial subepithelial fibrosis, a process which contributes to airway narrowing in asthma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / biosynthesis*
  • Allergens / immunology*
  • Asthma / immunology
  • Asthma / metabolism*
  • Biomarkers
  • Bronchi / cytology
  • Bronchi / drug effects*
  • Bronchi / immunology
  • Cell Differentiation / drug effects
  • Cells, Cultured
  • Culture Media
  • Endothelin-1 / pharmacology*
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Fibroblasts / immunology
  • Humans
  • Immunohistochemistry
  • Recombinant Proteins / pharmacology

Substances

  • Actins
  • Allergens
  • Biomarkers
  • Culture Media
  • Endothelin-1
  • Recombinant Proteins