ArticleJournal of theoretical biology2010
A mathematical model of intercellular signaling during epithelial wound healing.
Article in Journal of theoretical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Mathematical modeling of ventilator-induced lung inflammation.Journal of theoretical biology · 2021Article
- INVESTIGATION OF A STRUCTURED FISHER'S EQUATION WITH APPLICATIONS IN BIOCHEMISTRY.SIAM journal on applied mathematics · 2018Article
- Modeling keratinocyte wound healing dynamics: Cell-cell adhesion promotes sustained collective migration.Journal of theoretical biology · 2016Article
- Using an Agent-Based Model to Examine the Role of Dynamic Bacterial Virulence Potential in the Pathogenesis of Surgical Site Infection.Advances in wound care · 2013Article
- Tracking monotonically advancing boundaries in image sequences using graph cuts and recursive kernel shape priors.IEEE transactions on medical imaging · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Recent experiments monitoring the healing process of wounded epithelial monolayers have demonstrated the necessity of MAPK activation for coordinated cell movement after damage. This MAPK activity is characterized by two wave-like phenomena. One MAPK "wave" that originates immediately after injury, propagates deep into the cell sheet, away from the edge, and then rebounds back to the wound interface. After this initial MAPK activity has largely disappeared, a second MAPK front propagates slowly from the wound interface and also continues into the cell sheet, maintaining a sustained level of MAPK activity throughout the cell sheet. It has been suggested that the first wave is initiated by Reactive Oxygen Species (ROS) generated at the time of injury. In this work, we develop a minimal mathematical model that reproduces the observed behavior. The main ingredients of our model are a competition between ligand (e.g., Epithelial Growth Factor) and ROS for the activation of Epithelial Growth Factor Receptor, and a feedback loop between receptor occupancy and MAPK activation. We explore the mathematical properties of the model and look for traveling wave solutions consistent with the experimentally observed MAPK activity patterns.
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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.