Evidence map›Paper›PMID 20940302›Full record

ArticleThe Journal of biological chemistry2010

Inactivation of adenosine A2A receptor attenuates basal and angiotensin II-induced ROS production by Nox2 in endothelial cells.

Sapna Thakur, Junjie Du, Susanna Hourani, Catherine Ledent, Jian-Mei Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Adenosine ABiomedicines · 2020
    Article
  10. CD73Journal of extracellular vesicles · 2020
    Article
  11. Inactivation of endothelial adenosine ABritish journal of pharmacology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Adenosine AMolecular medicine (Cambridge, Mass.) · 2018
    Article
  19. Article
  20. Article
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

5 authors at 2 institutions in 2 countries.

Sapna ThakurFaculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, United Kingdom.
Junjie Du
Susanna Hourani
Catherine Ledent
Jian-Mei Li
University of Surrey · GBUniversité Libre de Bruxelles · BE

Funding

British Heart Foundation 078637/Z/05/Z.British Heart Foundation PG/06/073/21118Wellcome TrustWellcome Trust 078637/Z/05/Z
6 · The paper itself

Abstract

Endothelial cells (ECs) express a Nox2 enzyme, which, by generating reactive oxygen species (ROS), contributes to EC redox signaling and angiotensin II (AngII)-induced endothelial dysfunction. ECs also express abundantly an adenosine A(2A) receptor (A(2A)R), but its role in EC ROS production remains unknown. In this study, we investigated the role of A(2A)R in the regulation of Nox2 activity and signaling in ECs with or without acute AngII stimulation. In cultured ECs (SVEC4-10), AngII (100 nm, 30 min) significantly increased Nox2 membrane translocation and association with A(2A)R. These were accompanied by p47(phox), ERK1/2, p38 MAPK, and Akt phosphorylation and an increased ROS production (169 ± 0.04%). These AngII effects were inhibited back to the control levels by a specific A(2A)R antagonist (SCH58261), or adenosine deaminase, or by knockdown of A(2A)R or Nox2 using specific siRNAs. Knockdown of A(2A)R, as determined by Western blotting, decreased Nox2 and p47(phox) expression. In wild-type mouse aorta, SCH58261 significantly reduced acute AngII-induced ROS production and preserved endothelium-dependent vessel relaxation to acetylcholine. These results were further confirmed by using aortas from A(2A)R knock-out mice. In conclusion, A(2A)R is involved in the regulation of EC ROS production by Nox2. Inhibition or blockade of A(2A)R protects ECs from acute AngII-induced oxidative stress, MAPK activation, and endothelium dysfunction.

Indexed as

Adenosine A2 Receptor AntagonistsAngiotensin IIAnimalsCells, CulturedEndothelial CellsEnzyme ActivationGene Expression Regulation, EnzymologicMembrane GlycoproteinsMiceMice, KnockoutMitogen-Activated Protein Kinase 3NADPH Oxidase 2NADPH Oxidasesp38 Mitogen-Activated Protein KinasesPhosphorylationProto-Oncogene Proteins c-akt5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidineAdenosine A2 Receptor AntagonistsAngiotensin IICybb protein, mouseMembrane GlycoproteinsMitogen-Activated Protein Kinase 3NADPH Oxidase 2NADPH Oxidasesneutrophil cytosolic factor 1p38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktPyrimidinesReactive Oxygen SpeciesReceptor, Adenosine A2ATriazoles

Identifiers

PMID20940302
PMCPMC3000993
OpenAlexW2010902736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.