[Effect of salbutamol on proliferation of human bronchial epithelial cells: role of MAP kinase]

Nihon Kokyuki Gakkai Zasshi. 1998 May;36(5):428-32.
[Article in Japanese]

Abstract

To determine whether stimulation of beta-adrenoceptors affects proliferation of airway epithelial cells and, if so, whether activation of mitogen-activated protein kinase (MAPK) is involved, we studied cultured human bronchial epithelial (16-HBE) cells in vitro. The 16-HBE cells were grown to subconfluence in 96-well plates, and their growth was inhibited by incubation in serum-free medium for 72 h. The cells were ten incubated in the presence of saltbutamol (SAL, 10(-7) M), a specific beta(2)-adrenoceptor agonist. Proliferation of the cells was evaluated by MTT assay and total DNA content, and activation of MAPK was assessed by immunocytochemistry and Western blotting for phosphorylated MAPK (phospho-MAPK). Immunocytochemistry and immunoblots demonstrated that phospho-MAPK was expressed within minutes of SAL exposure. This effect of SAL was as potent as that of 10% serum, and was greatly inhibited by treatment with propranolol. These results suggest that SAL is a potent mitogen of airway epithelial cells and that its effect may be exerted by beta(2)-adrenocepter-mediated activation of MAPK.

Publication types

  • English Abstract

MeSH terms

  • Adrenergic beta-2 Receptor Agonists*
  • Adrenergic beta-Agonists / pharmacology*
  • Albuterol / pharmacology*
  • Bronchi / cytology*
  • Bronchi / metabolism
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Calcium-Calmodulin-Dependent Protein Kinases / physiology*
  • Cell Division / drug effects
  • Cells, Cultured
  • DNA / biosynthesis
  • Epithelial Cells / cytology*
  • Epithelial Cells / metabolism
  • Humans
  • Phosphorylation

Substances

  • Adrenergic beta-2 Receptor Agonists
  • Adrenergic beta-Agonists
  • DNA
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Albuterol