波形蛋白中间丝的丢失降低了核周围的硬度并增强了细胞通过受限空间的运动性
Loss of vimentin intermediate filaments decreases peri-nuclear stiffness and enhances cell motility through confined spaces
摘要：
细胞在组织中通过紧密收缩的空间或沿着纤维轨道的迁移对于生物过程（例如胚胎发生、伤口愈合和癌症转移）是重要的，并且取决于细胞骨架的机械性质。迁移细胞经常表达和上调中间丝蛋白波形蛋白。波形蛋白网络在剪切变形中的粘弹性已被证明，但其在运动性中的作用在很大程度上未被探索。在这里，我们研究了波形蛋白对细胞运动性和刚度的影响，使用小鼠胚胎成纤维细胞来自野生型和波形蛋白基因敲除小鼠。我们发现，波形蛋白的损失增加了通过小孔和沿薄毛细血管的运动性。原子力显微镜测量结果表明，波形蛋白的存在下，提高了细胞的核周刚度，在一定程度上，这取决于表面配体的介绍，因此从细胞外基质受体的信号。总之，我们的研究结果表明，波形蛋白通过提供对大应变的机械阻力来阻碍三维运动，从而保护细胞的结构完整性。
英文摘要：
The migration of cells through tight constricting spaces or along fibrous tracks in tissues is important for biological processes, such as embryogenesis, wound healing, and cancer metastasis, and depends on the mechanical properties of the cytoskeleton. Migratory cells often express and upregulate the intermediate filament protein vimentin. The viscoelasticity of vimentin networks in shear deformation has been documented, but its role in motility is largely unexplored. Here, we studied the effects of vimentin on cell motility and stiffness using mouse embryo fibroblasts derived from wild-type and vimentin-null mice. We find that loss of vimentin increases motility through small pores and along thin capillaries. Atomic force microscopy measurements reveal that the presence of vimentin enhances the perinuclear stiffness of the cell, to an extent that depends on surface ligand presentation and therefore signaling from extracellular matrix receptors. Together, our results indicate that vimentin hinders three-dimensional motility by providing mechanical resistance against large strains and may thereby protect the structural integrity of cells.
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