Evidence map›Paper›PMID 27828952›Full record

ArticlePloS one2016

Computational Screening of Tip and Stalk Cell Behavior Proposes a Role for Apelin Signaling in Sprout Progression.

Margriet M Palm, Marchien G Dallinga, Erik van Dijk, Ingeborg Klaassen, Reinier O Schlingemann, Roeland M H Merks

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Review
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  8. Cerebrovascular development: mechanisms and experimental approaches.Cellular and molecular life sciences : CMLS · 2021
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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

6 authors.

Margriet M PalmLife Sciences Group, Centrum Wiskunde & Informatica, Amsterdam, the Netherlands.
Marchien G DallingaOcular Angiogenesis Group, Academic Medical Center, Amsterdam, the Netherlands.
Erik van DijkLife Sciences Group, Centrum Wiskunde & Informatica, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-4745-2533
Ingeborg KlaassenOcular Angiogenesis Group, Academic Medical Center, Amsterdam, the Netherlands.
Reinier O SchlingemannOcular Angiogenesis Group, Academic Medical Center, Amsterdam, the Netherlands.
Roeland M H MerksLife Sciences Group, Centrum Wiskunde & Informatica, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-6152-687X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis involves the formation of new blood vessels by sprouting or splitting of existing blood vessels. During sprouting, a highly motile type of endothelial cell, called the tip cell, migrates from the blood vessels followed by stalk cells, an endothelial cell type that forms the body of the sprout. To get more insight into how tip cells contribute to angiogenesis, we extended an existing computational model of vascular network formation based on the cellular Potts model with tip and stalk differentiation, without making a priori assumptions about the differences between tip cells and stalk cells. To predict potential differences, we looked for parameter values that make tip cells (a) move to the sprout tip, and (b) change the morphology of the angiogenic networks. The screening predicted that if tip cells respond less effectively to an endothelial chemoattractant than stalk cells, they move to the tips of the sprouts, which impacts the morphology of the networks. A comparison of this model prediction with genes expressed differentially in tip and stalk cells revealed that the endothelial chemoattractant Apelin and its receptor APJ may match the model prediction. To test the model prediction we inhibited Apelin signaling in our model and in an in vitro model of angiogenic sprouting, and found that in both cases inhibition of Apelin or of its receptor APJ reduces sprouting. Based on the prediction of the computational model, we propose that the differential expression of Apelin and APJ yields a "self-generated" gradient mechanisms that accelerates the extension of the sprout.

Indexed as

AlgorithmsAnimalsApelinApelin ReceptorsBlood VesselsCell MovementChemotaxisComputational BiologyComputer SimulationEndothelial CellsHumansIntercellular Signaling Peptides and ProteinsModels, BiologicalNeovascularization, PhysiologicReceptors, G-Protein-CoupledRNA InterferenceApelinApelin ReceptorsAPLN protein, humanAPLNR protein, humanIntercellular Signaling Peptides and ProteinsKDR protein, humanReceptors, G-Protein-CoupledVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID27828952
PMCPMC5102492

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Registered trials

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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.