Evidence map›Paper›PMID 23637767›Full record

ArticlePloS one2013

Annexin peptide Ac2-26 suppresses TNFα-induced inflammatory responses via inhibition of Rac1-dependent NADPH oxidase in human endothelial cells.

Hitesh M Peshavariya, Caroline J Taylor, Celeste Goh, Guei-Sheung Liu, Fan Jiang, Elsa C Chan, Gregory J Dusting

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Loss of Endothelial Annexin A1 Aggravates Inflammation-Induched Vascular Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Annexin A1 involved in the regulation of inflammation and cell signaling pathways.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Antiinflammatory peptides: current knowledge and promising prospects.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  17. Article
  18. Article
  19. Review
  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

7 authors at 4 institutions in 2 countries.

Hitesh M PeshavariyaO'Brien Institute, University of Melbourne, Fitzroy, Victoria, Australia.
Caroline J Taylor
Celeste Goh
Guei-Sheung Liu
Fan Jiang
Elsa C Chan
Gregory J Dusting
O'Brien Institute · AUUniversity of Melbourne · AUAustralian Catholic University · AUQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anti-inflammatory peptide annexin-1 binds to formyl peptide receptors (FPR) but little is known about its mechanism of action in the vasculature. Here we investigate the effect of annexin peptide Ac2-26 on NADPH oxidase activity induced by tumour necrosis factor alpha (TNFα) in human endothelial cells. Superoxide release and intracellular reactive oxygen species (ROS) production from NADPH oxidase was measured with lucigenin-enhanced chemiluminescence and 2',7'-dichlorodihydrofluorescein diacetate, respectively. Expression of NADPH oxidase subunits and intracellular cell adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1) were determined by real-time PCR and Western blot analysis. Promoter activity of nuclear factor kappa B (NFκB) was measured by luciferase activity assay. TNFα stimulated NADPH-dependent superoxide release, total ROS formation and expression of ICAM-1and VCAM-1. Pre-treatment with N-terminal peptide of annexin-1 (Ac2-26, 0.5-1.5 µM) reduced all these effects, and the inhibition was blocked by the FPRL-1 antagonist WRW4. Furthermore, TNFα-induced NFκB promoter activity was attenuated by both Ac2-26 and NADPH oxidase inhibitor diphenyliodonium (DPI). Surprisingly, Nox4 gene expression was reduced by TNFα whilst expression of Nox2, p22phox and p67phox remained unchanged. Inhibition of NADPH oxidase activity by either dominant negative Rac1 (N17Rac1) or DPI significantly attenuated TNFα-induced ICAM-1and VCAM-1 expression. Ac2-26 failed to suppress further TNFα-induced expression of ICAM-1 and VCAM-1 in N17Rac1-transfected cells. Thus, Ac2-26 peptide inhibits TNFα-activated, Rac1-dependent NADPH oxidase derived ROS formation, attenuates NFκB pathways and ICAM-1 and VCAM-1 expression in endothelial cells. This suggests that Ac2-26 peptide blocks NADPH oxidase activity and has anti-inflammatory properties in the vasculature which contributes to modulate in reperfusion injury inflammation and vascular disease.

Indexed as

Annexin A1Anti-Inflammatory AgentsCells, CulturedEndothelial CellsEnzyme ActivationGene Expression RegulationHumansInflammationIntercellular Adhesion Molecule-1NADPH OxidasesNF-kappa BPeptidesPromoter Regions, Geneticrac1 GTP-Binding ProteinReceptors, Formyl PeptideReceptors, LipoxinAnnexin A1annexin A1 peptide (2-26)Anti-Inflammatory AgentsFPR2 protein, humanIntercellular Adhesion Molecule-1NADPH OxidasesNF-kappa BPeptidesrac1 GTP-Binding ProteinReceptors, Formyl PeptideReceptors, LipoxinSuperoxidesTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID23637767
PMCPMC3634803
OpenAlexW2167845253

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.