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Received for publication June 29, 2004.
Revised April 1, 2005.
Accepted for publication April 5, 2005.
Airway hyperresponsiveness (AHR) associated with heightened airway resistance and inflammation is the asthmatic characteristic feature. It has been demonstrated that contraclile responsiveness and Ca2+ sensitization to ACh in repeated antigen challenge-induced airway hyperresponsive bronchial preparation were significantly increased. The CPI-17 (PKC-potentiated inhibitory protein for heterotrimeric myosin light chain phosphatase of 17 kDa) is activated by PKC and acts on a myosin light chain phosphatase specific target. The aim of the present study was to explore the role of CPI-17 in hyperresponsiveness of bronchial smooth muscle in antigen-induced AHR rats. In immunoblotting, the levels of expression of CPI-17 mRNA and protein were significantly increased in bronchus from repeatedly antigen challenged rats. ACh-induced CPI-17 phosphorylation and translocation to membrane fraction were also significantly increased in bronchus from antigen-challenged rats. In conclusion, it is suggested that augmented expression and activation of CPI-17 observed in the hyperresponsive bronchial smooth muscle might be responsible for the enhanced ACh-induced Ca2+ sensitization of bronchial smooth muscle contraction associated with AHR.
Key words:
Muscarinic cholinergic, Protein Kinase C, Protein Kinases (other)
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