Evidence map›Paper›PMID 39768360›Full record

ArticleLife (Basel, Switzerland)2024

The Activation of the NF-κB Pathway in Human Adipose-Derived Stem Cells Alters the Deposition of Epigenetic Marks on H3K27 and Is Modulated by Fish Oil.

Jussara de Jesus Simao, Andressa França de Sousa Bispo, Victor Tadeu Gonçalves Plata, Ana Beatriz Marques Abel, Raphael Justa Saran, Júlia Fernandes Barcella, João Carlos Cardoso Alonso, André Valente Santana, Lucia Maria Armelin-Correa, Maria Isabel Cardoso Alonso-Vale

Abstract read
In one paragraph

Article in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
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  5. Review
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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

10 authors.

Jussara de Jesus SimaoPost-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.ORCID 0000-0001-8015-8278
Andressa França de Sousa BispoPost-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.ORCID 0000-0002-7698-710X
Victor Tadeu Gonçalves PlataPost-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.
Ana Beatriz Marques AbelPost-Graduate Program in Nutrition, Paulista School of Medicine, Federal University of São Paulo-UNIFESP, Sao Paulo 04023-062, Brazil.ORCID 0000-0003-2930-6321
Raphael Justa SaranDepartment of Biological Sciences, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.
Júlia Fernandes BarcellaDepartment of Biological Sciences, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.ORCID 0009-0000-1383-9065
João Carlos Cardoso AlonsoPaulínia Municipal Hospital, Paulínia 13140-000, Brazil.
André Valente SantanaPost-Graduate Program in Interdisciplinary Surgical Science, Paulista School of Medicine, Federal University of São Paulo-UNIFESP, Sao Paulo 04023-062, Brazil.
Lucia Maria Armelin-CorreaPost-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.ORCID 0000-0002-7200-5463
Maria Isabel Cardoso Alonso-ValePost-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.ORCID 0000-0001-5847-8080

Funding

Fundação de Amparo a Pesquisa - FAPESP #2019/13618-9
6 · The paper itself

Abstract

backgroundChronic low-grade inflammation in obesity is linked to white adipose tissue (WAT) dysfunction. Plasma lipopolysaccharide (LPS) activates Toll-like receptor 4 (TLR4), triggering NF-κB and worsening these disturbances. Previously, we showed that histone H3 lysine 27 (H3K27) epigenetic modifications affect WAT gene expression in high-fat-diet mice, identifying key pathways in adipose-derived stem cells (ASCs). This study explores whether NF-κB influences H3K27 modifiers in human ASCs and evaluates fish oil (FO) as a modulator.

methodsHuman visceral WAT ASCs were stimulated with LPS and treated with FO enriched with eicosapentaenoic acid (EPA). Flow cytometry, PCR array, RT-PCR, and Western blot assays were used.

resultsLPS increased NF-κB activity, elevating KDM6B demethylase levels and H3K27 acetylation. These epigenetic modifications in LPS-stimulated ASCs were associated with persistent changes in the expression of genes involved in adipogenesis, metabolic regulation, and inflammation, even after LPS removal and cell differentiation. FO mitigated these effects, reducing H3K27 acetylation and promoting methylation.

conclusionsFO demonstrates potential in modulating inflammation-induced epigenetic changes and preserving adipocyte function.

Indexed as

adipose tissueH3K27acH3K27me3inflammationKDM6Blipopolysaccharidemesenchymal stem cellsn-3 PUFA

Identifiers

PMID39768360
PMCPMC11678231

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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.