Evidence map›Paper›PMID 30597899›Full record

ArticleInternational journal of molecular sciences2018

NFκB Inhibition Mitigates Serum Amyloid A-Induced Pro-Atherogenic Responses in Endothelial Cells and Leukocyte Adhesion and Adverse Changes to Endothelium Function in Isolated Aorta.

Abigail Vallejo, Belal Chami, Joanne M Dennis, Martin Simone, Gulfam Ahmad, Adrian I Abdo, Arpeeta Sharma, Waled A Shihata, Nathan Martin, Jaye P F Chin-Dusting and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. 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
0.8field-weighted citation impact, top 34% 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, 15 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Evidence-based complementary and alternative medicine : eCAM · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019
    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

12 authors at 3 institutions in 1 country.

Abigail VallejoDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. aval3972@uni.sydney.edu.au.ORCID 0000-0001-5911-7308
Belal ChamiDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. belal.chami@sydney.edu.au.
Joanne M DennisDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. joanne.dennis@sydney.edu.au.
Martin SimoneDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. msim6013@uni.sydney.edu.au.
Gulfam AhmadDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. gulfam.ahmad@sydney.edu.au.
Adrian I AbdoHeart Research Institute, Newton, NSW 2053, Australia. adrian.abdo@hri.org.au.
Arpeeta SharmaBaker Heart and Diabetes Institute, Victoria 3004, Australia. Arpeeta.sharma@baker.edu.au.
Waled A ShihataBaker Heart and Diabetes Institute, Victoria 3004, Australia. waled.shihata@monash.com.au.
Nathan MartinDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. nmar7397@uni.sydney.edu.au.
Jaye P F Chin-DustingBaker Heart and Diabetes Institute, Victoria 3004, Australia. jaye.chin-dusting@baker.edu.au.
Judy B de HaanBaker Heart and Diabetes Institute, Victoria 3004, Australia. judy.dehaan@baker.edu.au.
Paul K WittingDiscipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW 2006, Australia. paul.witting@sydney.edu.au.
The University of Sydney · AUBaker Heart and Diabetes Institute · AUThe Heart Research Institute · AU

Funding

Australian Research Council DP160102063
6 · The paper itself

Abstract

The acute phase protein serum amyloid A (SAA) is associated with endothelial dysfunction and early-stage atherogenesis. Stimulation of vascular cells with SAA increases gene expression of pro-inflammation cytokines and tissue factor (TF). Activation of the transcription factor, nuclear factor kappa-B (NFκB), may be central to SAA-mediated endothelial cell inflammation, dysfunction and pro-thrombotic responses, while targeting NFκB with a pharmacologic inhibitor, BAY11-7082, may mitigate SAA activity. Human carotid artery endothelial cells (HCtAEC) were pre-incubated (1.5 h) with 10 μM BAY11-7082 or vehicle (control) followed by SAA (10 μg/mL; 4.5 h). Under these conditions gene expression for TF and Tumor Necrosis Factor (TNF) increased in SAA-treated HCtAEC and pre-treatment with BAY11-7082 significantly (TNF) and marginally (TF) reduced mRNA expression. Intracellular TNF and interleukin 6 (IL-6) protein also increased in HCtAEC supplemented with SAA and this expression was inhibited by BAY11-7082. Supplemented BAY11-7082 also significantly decreased SAA-mediated leukocyte adhesion to apolipoprotein E-deficient mouse aorta in

Indexed as

AnimalsAortaAtherosclerosisBiomarkersCell AdhesionEndothelial CellsEndothelium, VascularGene Expression RegulationHumansImmunohistochemistryInflammation MediatorsLeukocytesNF-kappa BRatsSerum Amyloid A ProteinBiomarkersInflammation MediatorsNF-kappa BSerum Amyloid A Proteinaortaatherosclerosisendotheliumnuclearserum amyloid Atranscription

Identifiers

PMID30597899
PMCPMC6337750
OpenAlexW2899469018

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.