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- Title
Acetylcholine-induced phosphorylation of CPI-17 in rat bronchial smooth muscle: the roles of Rho-kinase and protein kinase C.
- Authors
Sakai, Hiroyasu; Hirano, Tomona; Takeyama, Hisao; Chiba, Yoshihiko; Misawa, Miwa
- Abstract
It has been demonstrated that CPI-17 provokes an inhibition of myosin light chain phosphatase to increase myosin light chain phosphorylaton and Ca2+ sensitivity during contraction of vascular smooth muscle. However, expression and agonist-mediated regulation of CPI-17 in bronchial smooth muscle have not been documented. Thus, expression and phosphorylation of CPI-17 mediated by PKC and ROCK were investigated using rat bronchial preparations. Acetylcholine (ACh)-induced contraction and Ca2+ sensitization were both attenuated by 10–6 mol Y-27632 /L, a ROCK inhibitor, 10–6 mol calphostin C/L, a PKC inhibitor, and their combination. A PKC activator, PDBu, induced a Ca2+ sensitization in α-toxin-permeabilized bronchial smooth muscle. In this case, the Ca2+ sensitizing effect was significantly inhibited by caphostin C but not by Y-27632. An immunoblot study demonstrated CPI-17 expression in the rat bronchial smooth muscle. Acetylcholine induced a phosphorylation of CPI-17 in a concentration-dependent manner, which was significantly inhibited by Y-27632 and calphostin C. In conclusion, these data suggest that both PKC and ROCK are involved in force development, Ca2+ sensitization, and CPI-17 phosphorylation induced by ACh stimulation in rat bronchial smooth muscle. As such, RhoA/ROCK, PKC/CPI-17, and RhoA/ROCK/CPI pathways may play important roles in the ACh-induced Ca2+ sensitization of bronchial smooth muscle contraction.
- Subjects
SMOOTH muscle; BRONCHI; LUNGS; ACETYLCHOLINE; PROTEIN kinase C; PHOSPHORYLATION
- Publication
Canadian Journal of Physiology & Pharmacology, 2005, Vol 83, Issue 4, p375
- ISSN
0008-4212
- Publication type
Article
- DOI
10.1139/Y05-022