| First Author | Zhang WC | Year | 2010 |
| Journal | J Biol Chem | Volume | 285 |
| Issue | 8 | Pages | 5522-31 |
| PubMed ID | 20018858 | Mgi Jnum | J:159758 |
| Mgi Id | MGI:4452414 | Doi | 10.1074/jbc.M109.062836 |
| Citation | Zhang WC, et al. (2010) Myosin light chain kinase is necessary for tonic airway smooth muscle contraction. J Biol Chem 285(8):5522-31 |
| abstractText | Different interacting signaling modules involving Ca(2+)/calmodulin-dependent myosin light chain kinase, Ca(2+)-independent regulatory light chain phosphorylation, myosin phosphatase inhibition, and actin filament-based proteins are proposed as specific cellular mechanisms involved in the regulation of smooth muscle contraction. However, the relative importance of specific modules is not well defined. By using tamoxifen-activated and smooth muscle-specific knock-out of myosin light chain kinase in mice, we analyzed its role in tonic airway smooth muscle contraction. Knock-out of the kinase in both tracheal and bronchial smooth muscle significantly reduced contraction and myosin phosphorylation responses to K(+)-depolarization and acetylcholine. Kinase-deficient mice lacked bronchial constrictions in normal and asthmatic airways, whereas the asthmatic inflammation response was not affected. These results indicate that myosin light chain kinase acts as a central participant in the contractile signaling module of tonic smooth muscle. Importantly, contractile airway smooth muscles are necessary for physiological and asthmatic airway resistance. |
