ArticleAPL bioengineering2018
Fibroblast migration correlates with matrix softness. A study in knob-hole engineered fibrin.
Article in APL bioengineering, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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.
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Who cites it
6 citing papers in PubMed.
- The role of extracellular matrix stiffness in regulating fibroblast behaviors and disease progression.Frontiers in immunology · 2026Review
- Effects of biomechanical and biochemical stimuli on angio- and vasculogenesis in a complex microvasculature-on-chip.iScience · 2023Article
- The Mechanistic Understanding of RAD51 Defibrillation: A Critical Step in BRCA2-Mediated DNA Repair by Homologous Recombination.International journal of molecular sciences · 2022Article
- Optimization of Fibrin Scaffolds to Study Friction in Cultured Mesothelial Cells.International journal of molecular sciences · 2022Article
- Neonatal Fibrin Scaffolds Promote Enhanced Cell Adhesion, Migration, and Wound HealingCellular and molecular bioengineering · 2020Article
- Microfluidic-assisted preparation of RGD-decorated nanoparticles: exploring integrin-facilitated uptake in cancer cell lines.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The invasion of a matrix by migrating cells is a key step in its remodelling. At least in 2D migration models, cells tend to localize in stiffer areas (durotaxis). Here, we show that mechanical properties affect differently the 3D migration rate: non-proteolytic 3D cell migration is facilitated in softer matrices. In these gels, the modulus was varied by introducing defects in fibres, leaving largely intact the nanostructure. The matrices derive from fibrin via functionalization with a bioinert polymer [poly(ethylene glycol), PEG] through an affinity mechanism identical to that presiding to fibrin own self-assembly. Peptidic end groups on PEG were used to bind fibrinogen globular D regions [GPRP (glycine-proline-arginine-proline) for
Identifiers
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Registered trials
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.