Effect of protein kinase C on K(V) channel in rat bronchial smooth muscle.
- Author:
Xian-Sheng LIU
1
;
Yong-Jian XU
;
Zhen-Xiang ZHANG
;
Wang NI
;
Shi-Xin CHEN
Author Information
1. Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China. liuxiansheng@tih.tjmu.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Bronchi;
cytology;
Cells, Cultured;
Female;
Indoles;
pharmacology;
Kv1.5 Potassium Channel;
genetics;
physiology;
Male;
Membrane Potentials;
physiology;
Myocytes, Smooth Muscle;
cytology;
physiology;
Patch-Clamp Techniques;
Protein Kinase C;
metabolism;
physiology;
RNA, Messenger;
genetics;
metabolism;
Rats;
Rats, Sprague-Dawley;
Tetradecanoylphorbol Acetate;
pharmacology
- From:
Acta Physiologica Sinica
2003;55(2):135-141
- CountryChina
- Language: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.
