Matrix-degrading podosomes in smooth muscle cells
Matrix-degrading podosomes in smooth muscle cells
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DOI：
10.1016/j.ejcb.2005.08.001
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发表时间：
2006-04-01
影响因子：
6.6
通讯作者：
Gimona, M
中科院分区：
文献类型：
--
作者：
Lener, T;Burgstaller, G;Gimona, M
佛波酯对蛋白激酶C的激活可触发肌动蛋白细胞骨架的重塑和平滑肌细胞(SMC)中足小体的形成。在特定的微域对肌动蛋白动力学的区域控制导致局部收缩力量的减少。这种局部收缩抑制的分子基础包括足体形成过程中皮质蛋白的聚集(这在肌球蛋白、原肌球蛋白和H1降钙素的快速局部分散之前)，以及110 kDa肌动蛋白细丝相关蛋白(AFAP-110)和190 kDa Rho特异性GTP酶激活蛋白(P190RhoGAP)的特异性募集到微域。足体的形成还与细胞极化、细胞运动的诱导和细胞外基质的局部降解有关。这些发现可能为动脉粥样硬化病变和再狭窄发展过程中SMC侵袭的复杂机制提供解释，并支持基质降解和伴随的启动基于肌动蛋白的细胞运动的分子机制参与推动组织在平滑肌中侵袭的概念。(C)2005年爱思唯尔股份有限公司。版权所有。
Activation of protein kinase C by phorbol esters triggers the remodelling of the actin cytoskeleton and the formation of podosomes in smooth muscle cells (SMCs). Regional control of actin dynamics at specialised microdomains results in a local reduction in contractile forces. The molecular basis for this local inhibition of contractility includes the clustering of cortactin during podosome formation (which precedes the rapid, local dispersion of myosin, tropomyosin and h1 calponin), and the specific recruitment of 110-kDa actin filament-associated protein (AFAP- 110) and 190-kDa Rho-specific GTPase-activating protein (p190RhoGAP) to the microdomains. Podosome formation also correlates with cell polarisation, the induction of cell motility, and local degradation of the extracellular matrix. These findings may provide explanations for the complex mechanisms underlying SMC invasion in the course of the development of atherosclerotic lesions and restenosis, and support the concept that matrix degradation and the concomitant engagement of the molecular machinery initiating actin-based cell motility drive tissue invasion in smooth muscle. (c) 2005 Elsevier GmbH. All rights reserved.