Evidence map›Paper›PMID 29146905›Full record

ArticleNature communications2017

Pericytes regulate VEGF-induced endothelial sprouting through VEGFR1.

Hanna M Eilken, Rodrigo Diéguez-Hurtado, Inga Schmidt, Masanori Nakayama, Hyun-Woo Jeong, Hendrik Arf, Susanne Adams, Napoleone Ferrara, Ralf H Adams

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

166 citing papers in PubMed, 259 citations in OpenAlex.

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106 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Hanna M EilkenMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Rodrigo Diéguez-HurtadoMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Inga SchmidtMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Masanori NakayamaMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Hyun-Woo JeongMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Hendrik ArfMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Susanne AdamsMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Napoleone FerraraUniversity of California San Diego Medical Center, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
Ralf H AdamsMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, D-48149, Münster, Germany. ralf.adams@mpi-muenster.mpg.de.ORCID http://orcid.org/0000-0003-3031-7677
University of Münster · DEUniversity of California San Diego Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pericytes adhere to the abluminal surface of endothelial tubules and are required for the formation of stable vascular networks. Defective endothelial cell-pericyte interactions are frequently observed in diseases characterized by compromised vascular integrity such as diabetic retinopathy. Many functional properties of pericytes and their exact role in the regulation of angiogenic blood vessel growth remain elusive. Here we show that pericytes promote endothelial sprouting in the postnatal retinal vasculature. Using genetic and pharmacological approaches, we show that the expression of vascular endothelial growth factor receptor 1 (VEGFR1) by pericytes spatially restricts VEGF signalling. Angiogenic defects caused by pericyte depletion are phenocopied by intraocular injection of VEGF-A or pericyte-specific inactivation of the murine gene encoding VEGFR1. Our findings establish that pericytes promote endothelial sprouting, which results in the loss of side branches and the enlargement of vessels when pericyte function is impaired or lost.

Indexed as

AnimalsCapillariesCell LineDiphtheria ToxinEndothelial CellsEyeHeparin-binding EGF-like Growth FactorHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PhysiologicPericytesReceptor, Platelet-Derived Growth Factor betaRetinaDiphtheria ToxinFlt1 protein, mouseHeparin-binding EGF-like Growth FactorReceptor, Platelet-Derived Growth Factor betaVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID29146905
PMCPMC5691060
OpenAlexW2770491814

What OpenQuestion holds

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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.