Evidence map›Paper›PMID 27105673›Full record

ArticleJournal of theoretical biology2016

Modeling keratinocyte wound healing dynamics: Cell-cell adhesion promotes sustained collective migration.

John T Nardini, Douglas A Chapnick, Xuedong Liu, David M Bortz

Abstract read
In one paragraph

Article in Journal of theoretical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  10. Review
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  12. Article
  13. The Impact of Spaceflight and Simulated Microgravity on Cell Adhesion.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Journal of clinical medicine · 2019
    Article
  18. Article
  19. Article
  20. Engineering Approaches to Study Cellular Decision Making.Annual review of biomedical engineering · 2018
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

John T NardiniDepartment of Applied Mathematics, University of Colorado, Boulder, CO 80309-0526, United States; Interdisciplinary Quantitative Biology Graduate Program, University of Colorado, Boulder, CO 80309-0596, United States.
Douglas A ChapnickDepartment of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309-0596, United States. Electronic address: Douglas.Chapnick@colorado.edu.
Xuedong LiuDepartment of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309-0596, United States.
David M BortzDepartment of Applied Mathematics, University of Colorado, Boulder, CO 80309-0526, United States. Electronic address: dmbortz@colorado.edu.
University of Colorado Boulder · US

Funding

Mechanisms of p27Kipl Proteolysis in Cancer CellsR01CA107098 · NCI · UNIVERSITY OF COLORADO AT BOULDER · PI LIU, XUEDONG · 2004 to 2012
$2.7M
Quantitative Analysis of Mechanochemical Signaling in Wound ResponseR01AR068254 · NIAMS · UNIVERSITY OF COLORADO · PI LIU, XUEDONG · 2015 to 2021
$1.8M
ImageXpress Micro Cellular Imagining and Analysis SystemS10RR026680 · NCRR · UNIVERSITY OF COLORADO · PI LIU, XUEDONG · 2011 to 2011
$380k
NCI NIH HHS R01 CA107098NCRR NIH HHS S10 RR026680NIAMS NIH HHS R01 AR068254
6 · The paper itself

Abstract

The in vitro migration of keratinocyte cell sheets displays behavioral and biochemical similarities to the in vivo wound healing response of keratinocytes in animal model systems. In both cases, ligand-dependent Epidermal Growth Factor Receptor (EGFR) activation is sufficient to elicit collective cell migration into the wound. Previous mathematical modeling studies of in vitro wound healing assays assume that physical connections between cells have a hindering effect on cell migration, but biological literature suggests a more complicated story. By combining mathematical modeling and experimental observations of collectively migrating sheets of keratinocytes, we investigate the role of cell-cell adhesion during in vitro keratinocyte wound healing assays. We develop and compare two nonlinear diffusion models of the wound healing process in which cell-cell adhesion either hinders or promotes migration. Both models can accurately fit the leading edge propagation of cell sheets during wound healing when using a time-dependent rate of cell-cell adhesion strength. The model that assumes a positive role of cell-cell adhesion on migration, however, is robust to changes in the leading edge definition and yields a qualitatively accurate density profile. Using RNAi for the critical adherens junction protein, α-catenin, we demonstrate that cell sheets with wild type cell-cell adhesion expression maintain migration into the wound longer than cell sheets with decreased cell-cell adhesion expression, which fails to exhibit collective migration. Our modeling and experimental data thus suggest that cell-cell adhesion promotes sustained migration as cells pull neighboring cells into the wound during wound healing.

Indexed as

AlgorithmsModels, Biologicalalpha CateninCell AdhesionCell LineCell MovementComputer SimulationEpidermal Growth FactorErbB ReceptorsHumansKeratinocytesKineticsRNA InterferenceTime FactorsWound Healingalpha CateninEpidermal Growth FactorErbB ReceptorsCell–cell adhesionCollective migrationEpidermal growth factorKeratinocytesNonlinear diffusion equationsRe-epithelializationWound healing assays

Identifiers

PMID27105673
PMCPMC6089377
OpenAlexW2337617202

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.