Evidence map›Paper›PMID 26824355›Full record

ArticlePloS one2016

The GTPase ARF6 Controls ROS Production to Mediate Angiotensin II-Induced Vascular Smooth Muscle Cell Proliferation.

Mohamed Bourmoum, Ricardo Charles, Audrey Claing

Open access · goldAbstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.1field-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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  4. Acta pharmaceutica Sinica. B · 2022
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  7. Review
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  11. CLIC4/Arf6 Pathway.Circulation research · 2019
    Article
  12. Review
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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

3 authors at 1 institution in 1 country.

Mohamed BourmoumDepartment of Pharmacology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, H3T 1J4, Canada.
Ricardo CharlesDepartment of Pharmacology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, H3T 1J4, Canada.
Audrey ClaingDepartment of Pharmacology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, H3T 1J4, Canada.
Université de Montréal · CA

Funding

Canadian Institutes of Health Research MOP-79470
6 · The paper itself

Abstract

High reactive oxygen species (ROS) levels and enhanced vascular smooth muscle cells (VSMC) proliferation are observed in numerous cardiovascular diseases. The mechanisms by which hormones such as angiotensin II (Ang II) acts to promote these cellular responses remain poorly understood. We have previously shown that the ADP-ribosylation factor 6 (ARF6), a molecular switch that coordinates intracellular signaling events can be activated by the Ang II receptor (AT1R). Whether this small GTP-binding protein controls the signaling events leading to ROS production and therefore Ang II-dependent VSMC proliferation, remains however unknown. Here, we demonstrate that in rat aortic VSMC, Ang II stimulation led to the subsequent activation of ARF6 and Rac1, a key regulator of NADPH oxidase activity. Using RNA interference, we showed that ARF6 is essential for ROS generation since in conditions where this GTPase was knocked down, Ang II could no longer promote superoxide anion production. In addition to regulating Rac1 activity, ARF6 also controlled expression of the NADPH oxidase 1 (Nox 1) as well as the ability of the EGFR to become transactivated. Finally, ARF6 also controlled MAPK (Erk1/2, p38 and Jnk) activation, a key pathway of VSMC proliferation. Altogether, our findings demonstrate that Ang II promotes activation of ARF6 to controls ROS production by regulating Rac1 activation and Nox1 expression. In turn, increased ROS acts to activate the MAPK pathway. These signaling events represent a new molecular mechanism by which Ang II can promote proliferation of VSMC.

Indexed as

ADP-Ribosylation Factor 6ADP-Ribosylation FactorsAngiotensin IIAnimalsCell LineCell ProliferationErbB ReceptorsGene Expression RegulationMAP Kinase Kinase 4Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Muscle, Smooth, VascularMyocytes, Smooth MuscleNADH, NADPH OxidoreductasesNADPH Oxidase 1p38 Mitogen-Activated Protein KinasesADP-Ribosylation Factor 6ADP-Ribosylation FactorsAngiotensin IIArf6 protein, ratEgfr protein, ratErbB ReceptorsMAP Kinase Kinase 4Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADH, NADPH OxidoreductasesNADPH Oxidase 1NOX1 protein, ratp38 Mitogen-Activated Protein Kinasesrac1 GTP-Binding ProteinRac1 protein, ratReactive Oxygen SpeciesReceptor, Angiotensin, Type 1RNA, Small InterferingVasoconstrictor Agents

Identifiers

PMID26824355
PMCPMC4732744
OpenAlexW2273365605

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.