Effect of chronic cigarette smoking on large-conductance calcium-activated potassium channel and Kv1.5 expression in bronchial smooth muscle cells of rats.
- Author:
Hong YE
1
;
Wan-Li MA
;
Mu-Lan YANG
;
Sheng-Yuan LIU
;
Di-Xun WANG
Author Information
1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Pulmonary Disease Laboratory, Ministry of Health of China, Wuhan 430030, China. yehongmwl@hotmail.com
- Publication Type:Journal Article
- MeSH:
Animals;
Bronchi;
metabolism;
Cells, Cultured;
Kv1.5 Potassium Channel;
Male;
Muscle, Smooth;
cytology;
metabolism;
Potassium Channels, Calcium-Activated;
biosynthesis;
genetics;
Potassium Channels, Voltage-Gated;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Rats;
Rats, Sprague-Dawley;
Smoking;
adverse effects
- From:
Acta Physiologica Sinica
2004;56(5):573-578
- CountryChina
- Language:English
-
Abstract:
To investigate the role of potassium channels in the pathogenesis of airway hyperresponsiveness induced by cigarette smoking, the alteration in expression of large-conductance calcium-activated potassium channel (BKca) and voltage-dependent delayed rectifier potassium channel (Kv1.5) in bronchial smooth muscle cells were investigated in chronic cigarette smoking rats. Airway responsiveness was determined, hematoxylin and eosin staining, immuno-histochemistry, in-situ hybridization and western blot techniques were used. The results showed: (1) Chronic cigarette smoking down-regulated the protein synthesis and mRNA expression of BKca and Kv1.5 in bronchial and bronchiolar smooth muscles. (2) BKca decreased more markedly than Kv1.5 in bronchi, but there was no difference between them in bronchioli. (3) No changes in the expression of these two potassium channel proteins were found in extracted cell membrane protein from lung tissue. The results suggest that chronic cigarette smoking can down-regulate the levels of BKca and Kv1.5 in rat bronchial smooth muscle cells in vivo, which might contribute to the mechanism of airway hyperresponsiveness induced by cigarette smoking.
