Evidence map›Paper›PMID 22087332›Full record

ArticlePloS one2011

A two-compartment model of VEGF distribution in the mouse.

Phillip Yen, Stacey D Finley, Marianne O Engel-Stefanini, Aleksander S Popel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Phillip YenDepartment of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Stacey D Finley
Marianne O Engel-Stefanini
Aleksander S Popel
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Systems Biology of Angiogenesis in Peripheral Arterial DiseaseR01HL101200 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI POPEL, ALEKSANDER S. · 2010 to 2022
$10.7M
Predictive experiment-based multiscale models of the tumor immune microenvironment and immunotherapy in breast cancerR01CA138264 · NCI · JOHNS HOPKINS UNIVERSITY · PI POPEL, ALEKSANDER S. · 2009 to 2023
$8.1M
NCI NIH HHS R01 CA138264NHLBI NIH HHS R01 HL101200
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis--the growth of new microvessels from existing microvasculature. Angiogenesis is a complex process involving numerous molecular species, and to better understand it, a systems biology approach is necessary. In vivo preclinical experiments in the area of angiogenesis are typically performed in mouse models; this includes drug development targeting VEGF. Thus, to quantitatively interpret such experimental results, a computational model of VEGF distribution in the mouse can be beneficial. In this paper, we present an in silico model of VEGF distribution in mice, determine model parameters from existing experimental data, conduct sensitivity analysis, and test the validity of the model. The multiscale model is comprised of two compartments: blood and tissue. The model accounts for interactions between two major VEGF isoforms (VEGF(120) and VEGF(164)) and their endothelial cell receptors VEGFR-1, VEGFR-2, and co-receptor neuropilin-1. Neuropilin-1 is also expressed on the surface of parenchymal cells. The model includes transcapillary macromolecular permeability, lymphatic transport, and macromolecular plasma clearance. Simulations predict that the concentration of unbound VEGF in the tissue is approximately 50-fold greater than in the blood. These concentrations are highly dependent on the VEGF secretion rate. Parameter estimation was performed to fit the simulation results to available experimental data, and permitted the estimation of VEGF secretion rate in healthy tissue, which is difficult to measure experimentally. The model can provide quantitative interpretation of preclinical animal data and may be used in conjunction with experimental studies in the development of pro- and anti-angiogenic agents. The model approximates the normal tissue as skeletal muscle and includes endothelial cells to represent the vasculature. As the VEGF system becomes better characterized in other tissues and cell types, the model can be expanded to include additional compartments and vascular elements.

Indexed as

Models, BiologicalAngiogenesis InhibitorsAngiogenic ProteinsAnimalsBloodMiceNeuropilin-1Peptide FragmentsProtein BindingTissue DistributionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Angiogenesis InhibitorsAngiogenic ProteinsNeuropilin-1Peptide FragmentsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID22087332
PMCPMC3210788
OpenAlexW1999731963

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.