Document Detail


Cell crawling mediates collective cell migration to close undamaged epithelial gaps.
MedLine Citation:
PMID:  22711834     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 μm 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.
Authors:
Ester Anon; Xavier Serra-Picamal; Pascal Hersen; Nils C Gauthier; Michael P Sheetz; Xavier Trepat; Benoît Ladoux
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-06-18
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  109     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-07-04     Completed Date:  2012-09-18     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10891-6     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Actomyosin / physiology
Animals
Cell Count
Cell Culture Techniques / instrumentation,  methods
Cell Line
Cell Movement / physiology*
Dogs
Epithelial Cells / cytology*,  physiology*
Intercellular Junctions / physiology
Kidney / cytology
Myosin-Light-Chain Kinase / physiology
Pseudopodia / physiology*
Stress, Mechanical
Wound Healing / physiology*
rho-Associated Kinases / physiology
Grant Support
ID/Acronym/Agency:
242993//European Research Council
Chemical
Reg. No./Substance:
9013-26-7/Actomyosin; EC 2.7.11.1/rho-Associated Kinases; EC 2.7.11.18/Myosin-Light-Chain Kinase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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