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Forces driving epithelial wound healing

A. Brugues,Ester Anon,Vito Conte,J. Veldhuis,Mukund Gupta,J. Colombelli,J. Muñoz,G. Brodland,Benoit Ladoux,Benoit Ladoux,X. Trepat

Published 2014 in Nature Physics

ABSTRACT

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. Wound repair is thought to involve cell migration and the contraction of a tissue-level biopolymer ring—invoking analogy with the pulling of purse strings. Traction-force measurements now show that this ring engages the tissue's surroundings to steer migration, prompting revision of the purse-string mechanism.

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