Evidence map›Paper›PMID 26051942›Full record

ArticleCell reports2015

NRP1 Regulates CDC42 Activation to Promote Filopodia Formation in Endothelial Tip Cells.

Alessandro Fantin, Anastasia Lampropoulou, Gaia Gestri, Claudio Raimondi, Valentina Senatore, Ian Zachary, Christiana Ruhrberg

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

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  18. Fibrillin-1 regulates endothelial sprouting during angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023
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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Alessandro FantinUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Anastasia LampropoulouUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Gaia GestriUCL Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.
Claudio RaimondiUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Valentina SenatoreUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Ian ZacharyUCL Division of Medicine, University College London, 5 University Street, London WC1E 6JJ, UK.
Christiana RuhrbergUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK. Electronic address: c.ruhrberg@ucl.ac.uk.
University College London · GBUniversity College Hospital · GB

Funding

British Heart Foundation 095623/Z/11/ZBritish Heart Foundation FS/13/35/30148British Heart Foundation FS/13/60/30457British Heart Foundation PG/10/86/28622British Heart Foundation PG/11/61/29008British Heart Foundation RG/06/003/21131British Heart Foundation RG/11/11/29050Medical Research Council MR/L003775/1Wellcome Trust 095623
6 · The paper itself

Abstract

Sprouting blood vessels are led by filopodia-studded endothelial tip cells that respond to angiogenic signals. Mosaic lineage tracing previously revealed that NRP1 is essential for tip cell function, although its mechanistic role in tip cells remains poorly defined. Here, we show that NRP1 is dispensable for genetic tip cell identity. Instead, we find that NRP1 is essential to form the filopodial bursts that distinguish tip cells morphologically from neighboring stalk cells, because it enables the extracellular matrix (ECM)-induced activation of CDC42, a key regulator of filopodia formation. Accordingly, NRP1 knockdown and pharmacological CDC42 inhibition similarly impaired filopodia formation in vitro and in developing zebrafish in vivo. During mouse retinal angiogenesis, CDC42 inhibition impaired tip cell and vascular network formation, causing defects that resembled those due to loss of ECM-induced, but not VEGF-induced, NRP1 signaling. We conclude that NRP1 enables ECM-induced filopodia formation for tip cell function during sprouting angiogenesis.

Indexed as

Animalscdc42 GTP-Binding ProteinEmbryo, MammalianEndothelial CellsImmunohistochemistryMiceNeovascularization, PhysiologicNeuropilin-1PseudopodiaRhombencephalonSignal TransductionZebrafishcdc42 GTP-Binding ProteinCdc42 protein, mouseNeuropilin-1

Identifiers

PMID26051942
PMCPMC4528263
OpenAlexW1517374164

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.