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非肌肉肌球蛋白对平滑肌收缩表型的调控

Regulation of the smooth muscle contractile phenotype by nonmuscle myosin.

作者信息

Ogut Ozgur, Yuen Samantha L, Brozovich Frank V

机构信息

Cardiovascular Diseases, Mayo Medical School, 200 1st Street SW, Rochester, MN 55905, USA.

出版信息

J Muscle Res Cell Motil. 2007;28(7-8):409-14. doi: 10.1007/s10974-008-9132-2. Epub 2008 Mar 18.

Abstract

The contractile phenotype of a smooth muscle can broadly be classified as phasic or tonic. Following activation, phasic smooth muscle exhibits an initial period of rapid force activation, following which force falls to a lower steady state level. In contrast, force generated by tonic smooth muscle rises slowly to a sustained steady state. The differences in contractile patterns cannot be explained by the time course of either the Ca(2+) transient or phosphorylation of the 20-kDa regulatory myosin light chain (MLC(20)). Therefore, a molecular marker that defines tonic and phasic smooth muscle contractile properties remains elusive. Further, smooth muscle can maintain force at low levels of MLC(20) phosphorylation; often referred to as the latch state. The mechanism for the latch state is unknown and has been hypothesized to be due to a number of mechanisms including the formation of slowly cycling dephosphorylated or latch cross-bridges (Hai and Murphy, Am J Physiol 253:H1365-H1371, 1988). This review will focus evidence suggesting that nonmuscle myosin IIB (NMIIB) are the latch cross-bridges in smooth muscle and NMIIB content could define the tonic contractile phenotype.

摘要

平滑肌的收缩表型大致可分为相性或紧张性。激活后,相性平滑肌表现出一个初始的快速力激活期,之后力降至较低的稳态水平。相比之下,紧张性平滑肌产生的力缓慢上升至持续的稳态。收缩模式的差异无法用Ca(2+)瞬变或20 kDa调节性肌球蛋白轻链(MLC(20))磷酸化的时间进程来解释。因此,定义紧张性和相性平滑肌收缩特性的分子标志物仍然难以捉摸。此外,平滑肌可以在低水平的MLC(20)磷酸化下维持力;这通常被称为闩锁状态。闩锁状态的机制尚不清楚,据推测是由于多种机制,包括形成缓慢循环的去磷酸化或闩锁横桥(Hai和Murphy,《美国生理学杂志》253:H1365-H1371,1988)。本综述将聚焦于表明非肌肉肌球蛋白IIB(NMIIB)是平滑肌中的闩锁横桥且NMIIB含量可定义紧张性收缩表型的证据。

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