Evidence map›Paper›PMID 21670849›Full record

ArticleMolecular medicine (Cambridge, Mass.)

BRAP Activates Inflammatory Cascades and Increases the Risk for Carotid Atherosclerosis.

Yi-Chu Liao, Yung-Song Wang, Yuh-Cherng Guo, Kouichi Ozaki, Toshihiro Tanaka, Hsiu-Fen Lin, Ming-Hong Chang, Ku-Chung Chen, Ming-Lung Yu, Sheng-Hsiung Sheu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 29% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Observational
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  7. Review
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  15. Model-based clustering of multi-tissue gene expression data.Bioinformatics (Oxford, England) · 2020
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  20. Associations ofNeuropsychiatric disease and treatment · 2019
    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

11 authors at 4 institutions in 2 countries.

Yi-Chu LiaoGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan Section of Neurology, Taichung Veterans General Hospital, Taichung, Taiwan.
Yung-Song Wang
Yuh-Cherng Guo
Kouichi Ozaki
Toshihiro Tanaka
Hsiu-Fen Lin
Ming-Hong Chang
Ku-Chung Chen
Ming-Lung Yu
Sheng-Hsiung Sheu
Suh-Hang Hank Juo
Kaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWRIKEN Center for Integrative Medical Sciences · JPTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The BRCA-1 associated protein gene (BRAP) was recently identified as a susceptibility gene for myocardial infarction (MI). In the present study we aimed to decipher the association between the BRAP polymorphism and carotid atherosclerosis and the mechanism underlying its proatherogenic effect. A total of 1749 stroke/MI-free volunteers received carotid ultrasonic examinations for the measurement of intima-medial thickness (IMT) and plaque. The promoter polymorphism rs11066001 was selected because it affects the transcription of BRAP. We found that the GG genotype was associated with a 1.58-fold increased risk for having at least one plaque compared to carrying the A allele (P = 0.021). When subjects were divided by the cutoff value of IMT above the mean plus 1 standard deviation, there was an overrepresentation of the GG genotype in the subjects with thicker IMT (P = 0.004). The expression of BRAP increased significantly when human aortic smooth muscle cells (HASMCs) were treated with lipopolysaccharide (LPS). HASMCs were transfected with small interfering RNA against BRAP or scrambled sequences before treatment with LPS. Knockdown of BRAP led to attenuated HASMC proliferation and reduced secretion of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in response to LPS. Downregulation of BRAP did not affect the protein levels of nuclear factor-κB (NF-κB), but prohibited its nuclear translocation. Coimmunoprecipitation experiments confirmed an interaction between BRAP and the two major components of the IKK signalosome, IκBβ and IKKβ. Collectively, BRAP conferred a risk for carotid plaque and IMT. Inflammatory stimuli upregulated BRAP expression, and BRAP activated inflammatory cascades by regulating NF-κB nuclear translocation.

Indexed as

Polymorphism, Single NucleotideAdultAgedAged, 80 and overAnimalsCarotid Artery DiseasesCells, CulturedChlorocebus aethiopsCOS CellsFemaleGene FrequencyGenotypeHEK293 CellsHumansI-kappa B ProteinsInflammationBRAP protein, humanI kappa B beta proteinI-kappa B ProteinsLipopolysaccharidesUbiquitin-Protein Ligases

Identifiers

PMID21670849
PMCPMC3188876
OpenAlexW107220021

What OpenQuestion holds

Textmetadata
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.