Evidence map›Paper›PMID 32193709›Full record

ArticleBiomechanics and modeling in mechanobiology2020

A hybrid model of intercellular tension and cell-matrix mechanical interactions in a multicellular geometry.

Lewis E Scott, Lauren A Griggs, Vani Narayanan, Daniel E Conway, Christopher A Lemmon, Seth H Weinberg

Open access · greenAbstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Physical models of embryonic epithelial healing.PLoS computational biology · 2026
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  10. Immunofluorescence Image Feature Analysis and Phenotype Scoring Pipeline for Distinguishing Epithelial-Mesenchymal Transition.Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada · 2021
    Article
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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

6 authors at 1 institution in 1 country.

Lewis E ScottDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Lauren A GriggsDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Vani NarayananDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Daniel E ConwayDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Christopher A LemmonDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Seth H WeinbergDepartment of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, USA. weinberg.147@osu.edu.ORCID http://orcid.org/0000-0003-1170-0419
Virginia Commonwealth University · US

Funding

Cell junction and nuclear forces as mediators of epithelial cell homeostasisR35GM119617 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI Daniel E Conway · 2016 to 2026
$4.5M
Mechanochemical Signaling Dynamics in Epithelial-Mesenchymal TransitionR01GM122855 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI LEMMON, CHRISTOPHER ANDREW, WEINBERG, SETH HOWARD · 2018 to 2021
$1.2M
NIGMS NIH HHS R01 GM122855NIGMS NIH HHS R01GM122855NIGMS NIH HHS R35 GM119617NIGMS NIH HHS R35GM119617
6 · The paper itself

Abstract

Epithelial cells form continuous sheets of cells that exist in tensional homeostasis. Homeostasis is maintained through cell-to-cell junctions that distribute tension and balance forces between cells and their underlying matrix. Disruption of tensional homeostasis can lead to epithelial-mesenchymal transition (EMT), a transdifferentiation process in which epithelial cells adopt a mesenchymal phenotype, losing cell-cell adhesion and enhancing cellular motility. This process is critical during embryogenesis and wound healing, but is also dysregulated in many disease states. To further understand the role of intercellular tension in spatial patterning of epithelial cell monolayers, we developed a multicellular computational model of cell-cell and cell-substrate forces. This work builds on a hybrid cellular Potts model (CPM)-finite element model to evaluate cell-matrix mechanical feedback of an adherent multicellular cluster. Cellular movement is governed by thermodynamic constraints from cell volume, cell-cell and cell-matrix contacts, and durotaxis, which arises from cell-generated traction forces on a finite element substrate. Junction forces at cell-cell contacts balance these traction forces, thereby producing a mechanically stable epithelial monolayer. Simulations were compared to in vitro experiments using fluorescence-based junction force sensors in clusters of cells undergoing EMT. Results indicate that the multicellular CPM model can reproduce many aspects of EMT, including epithelial monolayer formation dynamics, changes in cell geometry, and spatial patterning of cell-cell forces in an epithelial tissue.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression RegulationAlgorithmsAnimalsCell AdhesionCell CommunicationCell DifferentiationCell Line, TumorCell MovementComputer SimulationDogsElastic ModulusEpithelial CellsFluorescence Resonance Energy TransferHomeostasisHumansTransforming Growth Factor beta1Cell–cell junction forcesCell mechanicsCellular Potts modelEpithelial–mesenchymal transitionSpatial patterningTraction forces

Identifiers

PMID32193709
PMCPMC7502553
OpenAlexW3011231601

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.