ArticleBMC systems biology2011
An integrated mathematical model of thrombin-, histamine-and VEGF-mediated signalling in endothelial permeability.
Article in BMC systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
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- PETN-Induced Antioxidative Properties in Endothelial Cells as a Target for Secondary Prevention of Endothelial Dysfunction in Pregnancy.Frontiers in physiology · 2022Article
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- The innate immune response to ischemic injury: a multiscale modeling perspective.BMC systems biology · 2018Article
- A Novel Compound Targeting Protease Receptor 1 Activators for the Treatment of Glioblastoma.Frontiers in neurology · 2018Article
- Understanding the Causes and Implications of Endothelial Metabolic Variation in Cardiovascular Disease through Genome-Scale Metabolic Modeling.Frontiers in cardiovascular medicine · 2016Review
- Global changes of phospholipids identified by MALDI imaging mass spectrometry in a mouse model of Alzheimer's disease.Journal of lipid research · 2016Article
- Thrombin Activity and Thrombin Receptor in Rat Glioblastoma Model: Possible Markers and Targets for Intervention?Journal of molecular neuroscience : MN · 2015Article
- An in-silico model of lipoprotein metabolism and kinetics for the evaluation of targets and biomarkers in the reverse cholesterol transport pathway.PLoS computational biology · 2014Article
- Regulation of endothelial permeability and transendothelial migration of cancer cells by tropomyosin-1 phosphorylation.Vascular cell · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial permeability is involved in injury, inflammation, diabetes and cancer. It is partly regulated by the thrombin-, histamine-, and VEGF-mediated myosin-light-chain (MLC) activation pathways. While these pathways have been investigated, questions such as temporal effects and the dynamics of multi-mediator regulation remain to be fully studied. Mathematical modeling of these pathways facilitates such studies. Based on the published ordinary differential equation models of the pathway components, we developed an integrated model of thrombin-, histamine-, and VEGF-mediated MLC activation pathways.
resultsOur model was validated against experimental data for calcium release and thrombin-, histamine-, and VEGF-mediated MLC activation. The simulated effects of PAR-1, Rho GTPase, ROCK, VEGF and VEGFR2 over-expression on MLC activation, and the collective modulation by thrombin and histamine are consistent with experimental findings. Our model was used to predict enhanced MLC activation by CPI-17 over-expression and by synergistic action of thrombin and VEGF at low mediator levels. These may have impact in endothelial permeability and metastasis in cancer patients with blood coagulation.
conclusionOur model was validated against a number of experimental findings and the observed synergistic effects of low concentrations of thrombin and histamine in mediating the activation of MLC. It can be used to predict the effects of altered pathway components, collective actions of multiple mediators and the potential impact to various diseases. Similar to the published models of other pathways, our model can potentially be used to identify important disease genes through sensitivity analysis of signalling components.
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