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首页> 外文期刊>American Journal of Physiology >Dissociation of Crk-associated substrate from the vimentin network is regulated by p21-activated kinase on ACh activation of airway smooth muscle.
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Dissociation of Crk-associated substrate from the vimentin network is regulated by p21-activated kinase on ACh activation of airway smooth muscle.

机译：Crk相关底物从波形蛋白网络的解离是由p21激活激酶对气道平滑肌ACh激活的调节。

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摘要

The intermediate filament protein vimentin has been shown to be required for smooth muscle contraction. The adapter protein p130 Crk-associated substrate (CAS) participates in the signaling processes that regulate force development in smooth muscle. However, the interaction of vimentin filaments with CAS has not been well elucidated. In the present study, ACh stimulation of tracheal smooth muscle strips increased the ratio of soluble to insoluble vimentin (an index of vimentin disassembly) in association with force development. ACh activation also induced vimentin phosphorylation at Ser(56) as assessed by immunoblot analysis. More importantly, CAS was found in the cytoskeletal vimentin fraction, and the amount of CAS in cytoskeletal vimentin was reduced in smooth muscle strips on contractile stimulation. CAS redistributed from the myoplasm to the periphery during ACh activation of smooth muscle cells. The ACh-elicited decrease in CAS distribution in cytoskeletal vimentin was attenuated by the downregulation of p21-activated kinase (PAK) 1 with antisense oligodeoxynucleotides. Vimentin phosphorylation at this residue, the ratio of soluble to insoluble vimentin, and active force in smooth muscle strips induced by ACh were also reduced in PAK-depleted tissues. These results suggest that PAK may regulate CAS release from the vimentin intermediate filaments by mediating vimentin phosphorylation at Ser(56) and the transition of cytoskeletal vimentin to soluble vimentin. The PAK-mediated dissociation of CAS from the vimentin network may participate in the cellular processes that affect active force development during ACh activation of tracheal smooth muscle tissues.
机译：中间丝蛋白波形蛋白已被证明是平滑肌收缩所必需的。衔接蛋白p130 Crk相关底物（CAS）参与调节平滑肌力发展的信号传导过程。但是，波形蛋白丝与CAS的相互作用尚未得到很好的阐明。在本研究中，ACh刺激气管平滑肌条带增加了可溶与不可溶波形蛋白的比例（波形蛋白分解的指数），并伴随着力量的发展。如通过免疫印迹分析所评估，ACh激活还诱导Ser（56）处波形蛋白磷酸化。更重要的是，在细胞骨架波形蛋白部分中发现了CAS，而在收缩刺激下平滑肌条中细胞骨架波形蛋白中CAS的数量减少了。在平滑肌细胞ACh激活期间，CAS从肌质重新分布到周围。 ACh引起的细胞骨架波形蛋白中CAS分布的减少通过反义寡脱氧核苷酸对p21活化激酶（PAK）1的下调而减弱。在富含PAK的组织中，该残基的波形蛋白磷酸化，可溶性波形蛋白和不溶波形蛋白的比率以及ACh诱导的平滑肌条中的活性力也降低了。这些结果表明PAK可能通过介导Ser（56）处的波形蛋白磷酸化和细胞骨架波形蛋白向可溶性波形蛋白的转变来调节波形蛋白中间丝中CAS的释放。 PAK介导的波形蛋白网络从CAS的解离可能参与影响气管平滑肌组织ACh激活过程中主动力发展的细胞过程。

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