Evidence map›Paper›PMID 31929522›Full record

ArticlePLoS computational biology2020

The role of actin protrusion dynamics in cell migration through a degradable viscoelastic extracellular matrix: Insights from a computational model.

Tommy Heck, Diego A Vargas, Bart Smeets, Herman Ramon, Paul Van Liedekerke, Hans Van Oosterwyck

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

18 citing papers in PubMed, 135 citations in OpenAlex.

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  16. Tools for computational analysis of moving boundary problems in cellular mechanobiology.Wiley interdisciplinary reviews. Systems biology and medicine · 2020
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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 2 institutions in 3 countries.

Tommy HeckBiomechanics Section, KU Leuven, Leuven, Belgium.ORCID 0000-0002-7389-7467
Diego A VargasBiomechanics Section, KU Leuven, Leuven, Belgium.
Bart SmeetsMeBioS, KU Leuven, Leuven, Belgium.ORCID 0000-0001-8753-781X
Herman RamonMeBioS, KU Leuven, Leuven, Belgium.
Paul Van LiedekerkeINRIA de Paris and Sorbonne Universités UPMC Univ paris 6, LJLL Team Mamba, Paris, France.ORCID 0000-0002-9314-6281
Hans Van OosterwyckBiomechanics Section, KU Leuven, Leuven, Belgium.ORCID 0000-0002-2142-9717
KU Leuven · BEInstitut national de recherche en sciences et technologies du numérique · FR

Funding

European Research Council 308223
6 · The paper itself

Abstract

Actin protrusion dynamics plays an important role in the regulation of three-dimensional (3D) cell migration. Cells form protrusions that adhere to the surrounding extracellular matrix (ECM), mechanically probe the ECM and contract in order to displace the cell body. This results in cell migration that can be directed by the mechanical anisotropy of the ECM. However, the subcellular processes that regulate protrusion dynamics in 3D cell migration are difficult to investigate experimentally and therefore not well understood. Here, we present a computational model of cell migration through a degradable viscoelastic ECM. This model is a 2D representation of 3D cell migration. The cell is modeled as an active deformable object that captures the viscoelastic behavior of the actin cortex and the subcellular processes underlying 3D cell migration. The ECM is regarded as a viscoelastic material, with or without anisotropy due to fibrillar strain stiffening, and modeled by means of the meshless Lagrangian smoothed particle hydrodynamics (SPH) method. ECM degradation is captured by local fluidization of the material and permits cell migration through the ECM. We demonstrate that changes in ECM stiffness and cell strength affect cell migration and are accompanied by changes in number, lifetime and length of protrusions. Interestingly, directly changing the total protrusion number or the average lifetime or length of protrusions does not affect cell migration. A stochastic variability in protrusion lifetime proves to be enough to explain differences in cell migration velocity. Force-dependent adhesion disassembly does not result in faster migration, but can make migration more efficient. We also demonstrate that when a number of simultaneous protrusions is enforced, the optimal number of simultaneous protrusions is one or two, depending on ECM anisotropy. Together, the model provides non-trivial new insights in the role of protrusions in 3D cell migration and can be a valuable contribution to increase the understanding of 3D cell migration mechanics.

Indexed as

ActinsExtracellular MatrixModels, BiologicalCell MovementComputational BiologyComputer SimulationElasticityViscosityActins

Identifiers

PMID31929522
PMCPMC6980736
OpenAlexW2999677295

What OpenQuestion holds

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LicenceCC BY
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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.