期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 109, 期 27, 页码 10891-10896出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1117814109
关键词
epithelial cell migration; microfabrication; wound model assay; Madin-Darby canine kidney cells
资金
- Association pour la Recherche sur le Cancer
- Association Francaise Contre la Myopathie
- Agence Nationale de la Recherche
- Spanish Ministry for Science and Innovation [BFU2009-07595]
- European Research Council and MBI [242993]
- Fondation pour la Recherche Medicale
- European Research Council (ERC) [242993] Funding Source: European Research Council (ERC)
- ICREA Funding Source: Custom
Fundamental biological processes such as morphogenesis and wound healing involve the closure of epithelial gaps. Epithelial gap closure is commonly attributed either to the purse-string contraction of an intercellular actomyosin cable or to active cell migration, but the relative contribution of these two mechanisms remains unknown. Here we present a model experiment to systematically study epithelial closure in the absence of cell injury. We developed a pillar stencil approach to create well-defined gaps in terms of size and shape within an epithelial cell monolayer. Upon pillar removal, cells actively respond to the newly accessible free space by extending lamellipodia and migrating into the gap. The decrease of gap area over time is strikingly linear and shows two different regimes depending on the size of the gap. In large gaps, closure is dominated by lamellipodium-mediated cell migration. By contrast, closure of gaps smaller than 20 mu m was affected by cell density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a passive physical mechanism. By changing the shape of the gap, we observed that low-curvature areas favored the appearance of lamellipodia, promoting faster closure. Altogether, our results reveal that the closure of epithelial gaps in the absence of cell injury is governed by the collective migration of cells through the activation of lamellipodium protrusion.
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