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首页> 外文期刊>Cytoskeleton >Podosome dynamics and location in vascular smooth muscle cells require CLASP-dependent microtubule bending
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Podosome dynamics and location in vascular smooth muscle cells require CLASP-dependent microtubule bending

机译：血管平滑肌细胞的体动态和位置需要依赖CLASP的微管弯曲

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Extracellular matrix (ECM) remodeling during physiological processes is mediated by invasive protrusions called podosomes. Positioning and dynamics of podosomes define the extent of ECM degradation. Microtubules are known to be involved in podosome regulation, but the role of microtubule (MT) network configuration in podosome dynamics and positioning is not well understood. Here, we show that the arrangement of the microtubule network defines the pattern of podosome formation and relocation in vascular smooth muscle cells (VSMCs). We show that microtubule plus-end targeting facilitates de novo formation of podosomes, in addition to podosome remodeling. Moreover, specialized bent microtubules with plus ends reversed towards the cell center promote relocation of podosomes from the cell edge to the cell center, resulting in an evenly distributed podosome pattern. Microtubule bending is induced downstream of protein kinase C (PKC) activation and requires microtubule-stabilizing proteins known as cytoplasmic linker associated proteins (CLASPs) and retrograde actin flow. Similar to microtubule depolymerization, CLASP depletion by siRNA blocks microtubule bending and eliminates centripetal relocation of podosomes. Podosome relocation also coincides with translocation of podosome-stimulating kinesin KIF1C, which is known to move preferentially along CLASP-associated microtubules. These findings indicate that CLASP-dependent microtubule network configuration is critical to the cellular location and distribution of KIF1C-dependent podosomes. (c) 2016 Wiley Periodicals, Inc.
机译：生理过程中的细胞外基质（ECM）重塑是由称为足小体的侵入性突起介导的。足小体的定位和动力学决定了ECM降解的程度。已知微管参与足小体调节，但是微管（MT）网络配置在足小体动力学和定位中的作用尚不清楚。在这里，我们显示微管网络的排列方式定义了足小体形成和血管平滑肌细胞（VSMC）迁移的模式。我们显示，微管加末端靶向促进podosome的从头形成，除了podosome重塑。而且，具有朝着细胞中心反转的正末端的专门弯曲的微管促进了足小体从细胞边缘向细胞中心的重新定位，从而产生了均匀分布的足小体模式。微管弯曲是在蛋白激酶C（PKC）激活的下游引起的，需要微管稳定蛋白，称为细胞质接头相关蛋白（CLASPs）和逆行肌动蛋白流。类似于微管解聚，siRNA清除CLASP会阻止微管弯曲并消除足小体的向心重定位。足小体的重定位也与刺激足小体的驱动蛋白KIF1C的移位相吻合，KIF1C已知优先沿着CLASP相关的微管移动。这些发现表明，依赖CLASP的微管网络配置对于依赖KIF1C的足小体的细胞定位和分布至关重要。 （c）2016年威利期刊有限公司

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