ArticleProceedings of the National Academy of Sciences of the United States of America2012
Cell crawling mediates collective cell migration to close undamaged epithelial gaps.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 218 citations in OpenAlex.
- Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization.bioRxiv : the preprint server for biology · 2026Article
- Cell type-specific response to curvature controls tissue growth dynamics in biomaterial pores.Bioactive materials · 2026Article
- The basement membrane determines the choice of wound healing mechanism across wound scales in the basal eukaryoteMolecular biology of the cell · 2026Article
- Activation of the FAK-MAPK/ERK1 pathway promotes intestinal epithelial cell sheet migration during fistula tract repair.Scientific reports · 2026Article
- Physical models of embryonic epithelial healing.PLoS computational biology · 2026Review
- The Interplay Between Stiffness and Hyperglycemia on Diabetic Foot Ulcer Wound Closure.Cellular and molecular bioengineering · 2026Article
- Wound Healing Effects of Polyethylene Glycol Loxenatide via PI3K/AKT Pathway: In Vitro Evaluation in Human Keratinocytes.Journal of diabetes research · 2026Article
- Partial fluidization theory of collective cell migration.Communications physics · 2026Article
- Engineered In Vitro Platforms for Mechanochemical Control of Cell Migration.Cold Spring Harbor perspectives in biology · 2025Review
- Edge curvature drives endoplasmic reticulum reorganization and dictates epithelial migration mode.Nature cell biology · 2025Article
- Review
- Article
- Substrate stress relaxation regulates monolayer fluidity and leader cell formation for collectively migrating epithelia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Strings and topological defects govern ordering kinetics in endothelial cell layers.Nature physics · 2025Article
- A Lifeact-EGFP quail for studying actin dynamics in vivo.The Journal of cell biology · 2024Article
- Mechanical state transitions in the regulation of tissue form and function.Nature reviews. Molecular cell biology · 2024Review
- Mechanochemical dynamics of collective cells and hierarchical topological defects in multicellular lumens.Science advances · 2024Article
- Reepithelialization of Diabetic Skin and Mucosal Wounds Is Rescued by Treatment With Epigenetic Inhibitors.Diabetes · 2024Article
- Regeneration in calcareous sponge relies on 'purse-string' mechanism and the rearrangements of actin cytoskeleton.Cell and tissue research · 2023Article
- An effective device to enable consistent scratches for in vitro scratch assays.BMC biotechnology · 2023Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.