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首页> 美国卫生研究院文献>Cell Regulation >Vinculin regulates directionality and cell polarity in two- and three-dimensional matrix and three-dimensional microtrack migration
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Vinculin regulates directionality and cell polarity in two- and three-dimensional matrix and three-dimensional microtrack migration

机译：Vinculin调节二维和三维矩阵以及三维微通道迁移中的方向性和细胞极性

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During metastasis, cells can use proteolytic activity to form tube-like “microtracks” within the extracellular matrix (ECM). Using these microtracks, cells can migrate unimpeded through the stroma. To investigate the molecular mechanisms of microtrack migration, we developed an in vitro three-dimensional (3D) micromolded collagen platform. When in microtracks, cells tend to migrate unidirectionally. Because focal adhesions are the primary mechanism by which cells interact with the ECM, we examined the roles of several focal adhesion molecules in driving unidirectional motion. Vinculin knockdown results in the repeated reversal of migration direction compared with control cells. Tracking the position of the Golgi centroid relative to the position of the nucleus centroid reveals that vinculin knockdown disrupts cell polarity in microtracks. Vinculin also directs migration on two-dimensional (2D) substrates and in 3D uniform collagen matrices, as indicated by reduced speed, shorter net displacement, and decreased directionality in vinculin-deficient cells. In addition, vinculin is necessary for focal adhesion kinase (FAK) activation in three dimensions, as vinculin knockdown results in reduced FAK activation in both 3D uniform collagen matrices and microtracks but not on 2D substrates, and, accordingly, FAK inhibition halts cell migration in 3D microtracks. Together these data indicate that vinculin plays a key role in polarization during migration.
机译：在转移过程中，细胞可以利用蛋白水解活性在细胞外基质（ECM）中形成管状的“微通道”。使用这些微径，细胞可以不受阻碍地通过基质迁移。为了研究微径迁移的分子机制，我们开发了体外三维（3D）微模化胶原蛋白平台。当处于微径时，细胞倾向于单向迁移。由于粘着斑是细胞与ECM相互作用的主要机制，因此我们研究了几种粘着斑分子在驱动单向运动中的作用。与对照细胞相比，Vinculin敲低导致迁移方向的反复逆转。跟踪高尔基体质心相对于细胞核质心位置的结果表明，蛋白链敲低会破坏微径中的细胞极性。 Vinculin还可以在二维（2D）基质和3D均匀胶原基质中定向迁移，这是由于缺乏蛋白蛋白的细胞速度降低，净位移缩短，方向性降低所表明的。此外，纽蛋白对于三维粘附粘附激酶（FAK）激活是必需的，因为纽蛋白敲除会导致3D均匀胶原蛋白基质和微通道中的FAK激活减少，但在2D基质上却没有，并且相应地，FAK抑制会阻止FAK抑制细胞迁移。 3D微型轨道。这些数据加在一起表明，新蛋白在迁移过程中的极化过程中起着关键作用。

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