Evidence map›Paper›PMID 23233245›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2013

Modulation of inflammatory cytokines and mitogen-activated protein kinases by acetate in primary astrocytes.

Mahmoud L Soliman, Colin K Combs, Thad A Rosenberger

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 4 pooled it
2.8field-weighted citation impact, top 11% 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

48 citing papers in PubMed, 4 syntheses or guidelines pooled it, 82 citations in OpenAlex.

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  7. Regulating the crosstalk betweenFrontiers in immunology · 2026
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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

3 authors at 1 institution in 1 country.

Mahmoud L SolimanDepartment of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences, 501 North Columbia Road, Room 3742, Grand Forks, ND 58203, USA.
Colin K Combs
Thad A Rosenberger
University of North Dakota · US

Funding

TRPC1, CALCIUM AND PARKINSON'S DISEASEP20RR017699 · NCRR · UNIVERSITY OF NORTH DAKOTA · PI GROVE, BRYON D · 2002 to 2011
$19.7M
NCRR NIH HHS 5P20RR017699NCRR NIH HHS P20 RR017699
6 · The paper itself

Abstract

Acetate supplementation attenuates neuroglia activation in a rat model of neuroinflammation by a mechanism associated with an increase in brain acetyl-CoA, an alteration in histone acetylation, and reduction of interleukin (IL)-1β expression. We propose that reduced astroglial activation occurs by disrupting astrocyte-derived inflammatory signaling and cytokine release. Using primary astroglial cultures, we found that LPS (0-25 ng/ml, 4 h) increased tumor necrosis factor (TNF-α) and IL-1β in a concentration-dependent manner, which was reduced by treatment with sodium acetate (12 mM). LPS did not alter H3K9 acetylation or IL-6 levels, whereas acetate treatment increased H3K9 acetylation by 2-fold and decreased basal levels of IL-6 by 2-fold. Acetate treatment attenuated the LPS-induced increase in TNF-α mRNA, but did not reverse the mRNA levels of other pro-inflammatory cytokines. By contrast, LPS decreased TGF-β1 and IL-4 protein and TGF-β1 mRNA, all of which was reversed with acetate treatment. Further, we found that acetate treatment completely reversed LPS-induced phosphorylation of MAPK p38 and decreased basal levels of phosphorylated extracellular signal-regulated kinases1/2 (ERK1/2) by 2-fold. Acetate treatment also reversed LPS-elevated NF-κB p65, CCAAT/enhancer-binding protein beta protein levels, and reduced basal levels of phosphorylated NF-κB p65 at serine 536. These results suggest that acetate treatment has a net anti-inflammatory effect in LPS-stimulated astrocytes that is largely associated with a disruption in MAPK and NF-κB signaling.

Indexed as

AcetatesAcetylationAcetyl Coenzyme AAnimalsAstrocytesBlotting, WesternCCAAT-Enhancer-Binding ProteinsCells, CulturedCytokinesHistonesInflammationIn Situ Nick-End LabelingLipopolysaccharidesL-Lactate DehydrogenaseMAP Kinase Signaling SystemMiceAcetatesAcetyl Coenzyme ACCAAT-Enhancer-Binding ProteinsCytokinesHistonesLipopolysaccharidesL-Lactate DehydrogenaseMitogen-Activated Protein KinasesNF-kappa BRNA, Messenger

Identifiers

PMID23233245
PMCPMC3587660
OpenAlexW2053022788

What OpenQuestion holds

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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.