Evidence map›Paper›PMID 15908579›Full record

ArticleBiophysical journal2005

Computational model for cell migration in three-dimensional matrices.

Muhammad H Zaman, Roger D Kamm, Paul Matsudaira, Douglas A Lauffenburger

Abstract readEvaluation Study
In one paragraph

Article in Biophysical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
–field-weighted citation impact
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

96 citing papers in PubMed.

  1. Chemical compensation to mechanical loss in cell mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  10. Mechanical properties, andFrontiers in bioengineering and biotechnology · 2023
    Article
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  16. Review
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36 more citing papers are in PubMed but not listed here.

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.

Muhammad H ZamanWhitehead Institute for Biomedical Research, Biological Engineering Division, Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, 02142, USA. mhzaman@mit.edu
Roger D Kamm
Paul Matsudaira
Douglas A Lauffenburger

Funding

Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Subcellular Mechanotransduction in Vascular Smooth Muscle CellsP01HL064858 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KAMM, ROGER D. · 2001 to 2005
$7.6M
STRUCTURE/FUNCTION OF CH DOMAIN PROTEINSR01GM057418 · NIGMS · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI MATSUDAIRA, PAUL T. · 1998 to 2005
$2.0M
NCI NIH HHS 1-P50-CA112967-01NCI NIH HHS U54 CA112967NHLBI NIH HHS P01 HL064858NHLBI NIH HHS P01-HL064858NIGMS NIH HHS R01 GM057418NIGMS NIH HHS R01-GM57418
6 · The paper itself

Abstract

Although computational models for cell migration on two-dimensional (2D) substrata have described how various molecular and cellular properties and physiochemical processes are integrated to accomplish cell locomotion, the same issues, along with certain new ones, might contribute differently to a model for migration within three-dimensional (3D) matrices. To address this more complicated situation, we have developed a computational model for cell migration in 3D matrices using a force-based dynamics approach. This model determines an overall locomotion velocity vector, comprising speed and direction, for individual cells based on internally generated forces transmitted into external traction forces and considering a timescale during which multiple attachment and detachment events are integrated. Key parameters characterize cell and matrix properties, including cell/matrix adhesion and mechanical and steric properties of the matrix; critical underlying molecular properties are incorporated explicitly or implicitly. Model predictions agree well with experimental results for the limiting case of migration on 2D substrata as well as with recent experiments in 3D natural tissues and synthetic gels. Certain predicted features such as biphasic behavior of speed with density of matrix ligands for 3D migration are qualitatively similar to their 2D counterparts, but new effects generally absent in 2D systems, such as effects due to matrix sterics and mechanics, are now predicted to arise in many 3D situations. As one particular sample manifestation of these effects, the optimal levels of cell receptor expression and matrix ligand density yielding maximal migration are dependent on matrix mechanical compliance.

Indexed as

Models, BiologicalAnimalsCell MovementComputer SimulationElasticityExtracellular MatrixHumansStress, Mechanical

Identifiers

PMID15908579
PMCPMC1366623

What OpenQuestion holds

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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.