Evidence map›Paper›PMID 26878794›Full record

ArticleThe Journal of nutritional biochemistry2016

EGCG prevents PCB-126-induced endothelial cell inflammation via epigenetic modifications of NF-κB target genes in human endothelial cells.

Dandan Liu, Jordan T Perkins, Bernhard Hennig

Abstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  18. Temporal and Geographical Variation of Intestinal Ulcers in Grey Seals (Animals : an open access journal from MDPI · 2021
    Article
  19. Review
  20. The Role of Histone Protein Acetylation in Regulating Endothelial Function.Frontiers in cell and developmental biology · 2021
    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

3 authors at 1 institution in 1 country.

Dandan LiuSuperfund Research Center, University of Kentucky, Lexington, KY 40536; Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40536.
Jordan T PerkinsSuperfund Research Center, University of Kentucky, Lexington, KY 40536; Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40536.
Bernhard HennigSuperfund Research Center, University of Kentucky, Lexington, KY 40536; Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40536. Electronic address: bhennig@uky.edu.
University of Kentucky · US

Funding

Vascular Mechanisms of PCB-Induced Brain MetastasesP42ES007380 · NIEHS · UNIVERSITY OF KENTUCKY · PI PENNELL, KELLY G · 1997 to 2024
$47.8M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
NIEHS NIH HHS P42 ES007380NIEHS NIH HHS P42ES007380NIGMS NIH HHS 8 P20 GM103527NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

Anti-inflammatory polyphenols, such as epigallocatechin-3-gallate (EGCG), have been shown to protect against the toxicity of environmental pollutants. It is well known that bioactive food compounds such as polyphenols may exert their protection by modulating inflammatory pathways regulated through nuclear factor-kappa B (NF-κB) signaling. EGCG has been reported to inhibit NF-κB activation. We hypothesize that EGCG can protect against polychlorinated biphenyl (PCB)-induced endothelial inflammation in part through epigenetic regulation of NF-κB-regulated inflammatory genes. In order to test this hypothesis, human endothelial cells (EA.hy926) were exposed to physiologically relevant levels of coplanar PCB 126 and/or 15 or 30 μM of EGCG, followed by quantification of NF-κB subunit p65, histone acetyltransferase p300 and histone deacetylases (HDACs) accumulation through chromatin immunoprecipitation assay in the promoter region of inflammatory genes. In addition, the enrichment of the acetylated H3 was also quantified. PCB 126 exposure increased the expression of vascular inflammatory mediators, including interleukin (IL)-6, C-reactive protein, intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and IL-1α/β, which were prevented by pretreatment with EGCG. This inhibitory effect by EGCG correlated with abolished nuclear import of p65, decreased chromatin binding of p65 and p300, as well as increased chromatin binding of HDAC 1/2. Furthermore, EGCG induced hypoacetylation of H3, which accounts for deactivation of downstream genes. These data suggest that EGCG-induced epigenetic modifications can decrease PCB-induced vascular toxicity.

Indexed as

AcetylationCatechinCell LineCell NucleusChromatinEndothelium, VascularGene Expression RegulationHumansInflammationInflammation MediatorsPolychlorinated BiphenylsProtein TransportTranscription Factor RelA3,4,5,3',4'-pentachlorobiphenylCatechinChromatinepigallocatechin gallateInflammation MediatorsPolychlorinated BiphenylsTranscription Factor RelAEGCGHDACsp300p65PCB 126Vascular inflammation

Identifiers

PMID26878794
PMCPMC4757812
OpenAlexW1824369281

What OpenQuestion holds

Textmetadata
LicenceTDM
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.