Forces driving epithelial wound healing.
Forces driving epithelial wound healing.
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DOI：
10.1038/nphys3040
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发表时间：
2014-09
期刊：
影响因子：
19.6
通讯作者：
Trepat X
中科院分区：
文献类型：
--
作者：
Brugués A;Anon E;Conte V;Veldhuis JH;Gupta M;Colombelli J;Muñoz JJ;Brodland GW;Ladoux B;Trepat X
多细胞生物的一个基本特征是它们能够通过上皮细胞移动到受损区域来自我修复伤口。这种集体细胞运动通常归因于细胞爬行和细胞外肌动球蛋白环的“荷包”收缩的组合。在这里，我们通过直接的实验测量表明，这两种机制不足以解释伤口闭合过程中观察到的力模式。在该过程的早期阶段，领先的肌动蛋白突起产生远离伤口的牵引力，表明伤口闭合最初是由细胞爬行驱动的。在后期阶段，我们观察到指向伤口的牵引力的意外模式。这样的图案具有与伤口径向和切向的强力分量。我们发现，这些力的分量产生的张力传输的异质肌动球蛋白环的底层基板通过焦点粘连。本文报道的结构和机械组织为细胞提供了一种通过协同压缩底层基质来闭合伤口的机制。
A fundamental feature of multicellular organisms is their ability to self-repair wounds through the movement of epithelial cells into the damaged area. This collective cellular movement is commonly attributed to a combination of cell crawling and “purse-string” contraction of a supracellular actomyosin ring. Here we show by direct experimental measurement that these two mechanisms are insufficient to explain force patterns observed during wound closure. At early stages of the process, leading actin protrusions generate traction forces that point away from the wound, showing that wound closure is initially driven by cell crawling. At later stages, we observed unanticipated patterns of traction forces pointing towards the wound. Such patterns have strong force components that are both radial and tangential to the wound. We show that these force components arise from tensions transmitted by a heterogeneous actomyosin ring to the underlying substrate through focal adhesions. The structural and mechanical organization reported here provides cells with a mechanism to close the wound by cooperatively compressing the underlying substrate.