Evidence map›Paper›PMID 27270835›Full record

ArticleScientific reports2016

CdGAP/ARHGAP31, a Cdc42/Rac1 GTPase regulator, is critical for vascular development and VEGF-mediated angiogenesis.

Christine Caron, Jonathan DeGeer, Patrick Fournier, Philippe M Duquette, Vilayphone Luangrath, Hidetaka Ishii, Fereshteh Karimzadeh, Nathalie Lamarche-Vane, Isabelle Royal

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 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

9 authors at 4 institutions in 1 country.

Christine CaronCRCHUM - Centre de recherche du Centre Hospitalier de l'Université de Montréal and Institut du Cancer de Montréal, Montréal, Québec, Canada.
Jonathan DeGeerCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Patrick FournierCRCHUM - Centre de recherche du Centre Hospitalier de l'Université de Montréal and Institut du Cancer de Montréal, Montréal, Québec, Canada.
Philippe M DuquetteCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Vilayphone LuangrathCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Hidetaka IshiiCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Fereshteh KarimzadehCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Nathalie Lamarche-VaneCancer Research Program, Research Institute-McGill University Hospital Centre, Montreal, Quebec, Canada.
Isabelle RoyalCRCHUM - Centre de recherche du Centre Hospitalier de l'Université de Montréal and Institut du Cancer de Montréal, Montréal, Québec, Canada.
McGill University · CACentre Hospitalier de l’Université de Montréal · CAMcGill University Health Centre · CAUniversité de Montréal · CA

Funding

CIHR 292353CIHR MOP-119544CIHR MOP-93681
6 · The paper itself

Abstract

Mutations in the CdGAP/ARHGAP31 gene, which encodes a GTPase-activating protein for Rac1 and Cdc42, have been reported causative in the Adams-Oliver developmental syndrome often associated with vascular defects. However, despite its abundant expression in endothelial cells, CdGAP function in the vasculature remains unknown. Here, we show that vascular development is impaired in CdGAP-deficient mouse embryos at E15.5. This is associated with superficial vessel defects and subcutaneous edema, resulting in 44% embryonic/perinatal lethality. VEGF-driven angiogenesis is defective in CdGAP(-/-) mice, showing reduced capillary sprouting from aortic ring explants. Similarly, VEGF-dependent endothelial cell migration and capillary formation are inhibited upon CdGAP knockdown. Mechanistically, CdGAP associates with VEGF receptor-2 and controls VEGF-dependent signaling. Consequently, CdGAP depletion results in impaired VEGF-mediated Rac1 activation and reduced phosphorylation of critical intracellular mediators including Gab1, Akt, PLCγ and SHP2. These findings are the first to demonstrate the importance of CdGAP in embryonic vascular development and VEGF-induced signaling, and highlight CdGAP as a potential therapeutic target to treat pathological angiogenesis and vascular dysfunction.

Indexed as

AnimalsBlood Vesselscdc42 GTP-Binding ProteinGTPase-Activating ProteinsMiceMice, KnockoutNeovascularization, PhysiologicVascular Endothelial Growth Factor AArhgap31 protein, mousecdc42 GTP-Binding ProteinGTPase-Activating ProteinsVascular Endothelial Growth Factor A

Identifiers

PMID27270835
PMCPMC4895392
OpenAlexW2409810875

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.