[Effect of protein kinase C on K(V) channel in rat bronchial smooth muscle]

Sheng Li Xue Bao. 2003 Apr 25;55(2):135-41.
[Article in Chinese]

Abstract

The effect of protein kinase C (PKC) signaling pathway on the activity of voltage-dependent delayed rectifier potassium channel (K(V)) and the expression of K(V) isoform K(V)1.5 in rat bronchial smooth cells (BSMCs) were investigated with whole-cell patch clamp, Western-blot and RT-PCR techniques. The results showed: (1) phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a significant inhibition of K(V) channel currents in rat BSMCs. The inhibition was partly abolished by Ro31-8220, a PKC inhibitor. (2) PMA caused a significant suppression of the expression of K(V)1.5 mRNA and protein in rat BSMCs. These effects were attenuated by Ro31-8220. The results suggest that in rat BSMCs PKC activation inhibits K(V) currents and down-regulates the expression of K(V)1.5.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bronchi / cytology*
  • Cells, Cultured
  • Female
  • Indoles / pharmacology
  • Kv1.5 Potassium Channel / genetics
  • Kv1.5 Potassium Channel / physiology*
  • Male
  • Membrane Potentials / physiology
  • Myocytes, Smooth Muscle / cytology
  • Myocytes, Smooth Muscle / physiology*
  • Patch-Clamp Techniques
  • Protein Kinase C / metabolism
  • Protein Kinase C / physiology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Indoles
  • Kv1.5 Potassium Channel
  • RNA, Messenger
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate
  • Ro 31-8220