Evidence map›Paper›PMID 27345502›Full record

ArticleScientific reports2016

The insect repellent N,N-diethyl-m-toluamide (DEET) induces angiogenesis via allosteric modulation of the M3 muscarinic receptor in endothelial cells.

Samuel Legeay, Nicolas Clere, Grégory Hilairet, Quoc-Tuan Do, Philippe Bernard, Jean-François Quignard, Véronique Apaire-Marchais, Bruno Lapied, Sébastien Faure

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Exposure to N,N-diethyl-Frontiers in public health · 2022
    Article
  8. Review
  9. Narrative Review on Health-EDRM Primary Prevention Measures for Vector-Borne Diseases.International journal of environmental research and public health · 2020
    Review
  10. Article
  11. Article
  12. Review
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 3 institutions in 1 country.

Samuel LegeayUniversity Bretagne Loire, Université d'Angers, UFR santé, département pharmacie, Angers, France.
Nicolas ClereUniversity Bretagne Loire, Université d'Angers, UFR santé, département pharmacie, Angers, France.
Grégory HilairetUniversity Bretagne Loire, Université d'Angers, UFR santé, département pharmacie, Angers, France.
Quoc-Tuan DoGreenPharma S.A.S. 03 allée du titane, 45100 Orléans, France.
Philippe BernardGreenPharma S.A.S. 03 allée du titane, 45100 Orléans, France.
Jean-François QuignardInserm U1045-Centre de Recherche Cardio-Thoracique de Bordeaux, Université de Bordeaux, France.
Véronique Apaire-MarchaisLaboratoire des Récepteurs et Canaux Ioniques Membranaires (RCIM), UPRES-EA 2647, USC INRA 1330, Angers, France.
Bruno LapiedLaboratoire des Récepteurs et Canaux Ioniques Membranaires (RCIM), UPRES-EA 2647, USC INRA 1330, Angers, France.
Sébastien FaureUniversity Bretagne Loire, Université d'Angers, UFR santé, département pharmacie, Angers, France.
Laboratoire Stress Oxydant et Pathologies Métaboliques · FRSignalisation Fonctionnelle des Canaux Ioniques et Récepteurs · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insect repellent N,N-diethyl-m-toluamide (DEET) has been reported to inhibit AChE (acetylcholinesterase) and to possess potential carcinogenic properties with excessive vascularization. In the present paper, we demonstrate that DEET specifically stimulates endothelial cells that promote angiogenesis which increases tumor growth. DEET activates cellular processes that lead to angiogenesis including proliferation, migration and adhesion. This is associated with an enhancement of NO production and VEGF expression in endothelial cells. M3 silencing or the use of a pharmacological M3 inhibitor abrogates all of these effects which reveals that DEET-induced angiogenesis is M3 sensitive. The experiments involving calcium signals in both endothelial and HEK cells overexpressing M3 receptors, as well as binding and docking studies demonstrate that DEET acts as an allosteric modulator of the M3 receptor. In addition, DEET inhibited AChE which increased acetylcholine bioavailability and binding to M3 receptors and also strengthened proangiogenic effects by an allosteric modulation.

Indexed as

AcetylcholineAllosteric RegulationAnimalsBiological AvailabilityCalcium SignalingCell AdhesionCell LineCell Line, TumorCell MovementCell ProliferationDEETEndothelial CellsHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsInsect RepellentsAcetylcholineDEETInsect RepellentsReceptor, Muscarinic M3Vascular Endothelial Growth Factor A

Identifiers

PMID27345502
PMCPMC4921870
OpenAlexW2470566888

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.