期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 15, 期 -, 页码 750-764出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/3644
关键词
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资金
- NIH [HL71930, HL087401]
- Sepracor Inc
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL071930, R33HL087401] Funding Source: NIH RePORTER
Airway smooth muscle cell (ASMC) contraction is regulated by myosin phosphorylation to control actin-myosin cross-bridge activity. Myosin phosphorylation is determined by the antagonistic activity of myosin light chain (MLC) kinase (MLCK) and phosphatase (MLCP). MLCK activity is increased by increases in intracellular Ca2+ concentration ([Ca2+](i)) associated with Ca2+ oscillations. MLCP activity is decreased by phosphorylation of MLCP or accessory proteins by kinases, including Rho-kinase or protein kinase C. During agonist-induced ASMC contraction, these 2 pathways are simultaneously activated. Because MLCP activity is often independent of [Ca2+](i), changes in MLCP activity can alter ASMC tone at a constant [Ca2+](i); a behavior termed Ca2+ sensitivity. In asthma, airway hyperresponsiveness (AHR) may result from an increase in the Ca2+-dependent contractile mechanisms and/or the Ca2+ sensitivity of ASMCs. Conversely, inhalation of beta2-adrenergic agonists induce airway relaxation by simultaneously slowing the Ca2+ oscillations and reducing the Ca2+ sensitivity of ASMCs. However, the action of beta2-adrenergic agonists varies with species. Consequently, the development of beta2-adrenergic agonists requires a characterization of their action in human airways.
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