Cited by 131Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersNeuroscience and Neuropharmacology Research

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Acetate reduces microglia inflammatory signaling in vitro

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Soliman, Mahmoud L., Puig, Kendra L., Combs, Colin K., Rosenberger, Thad A.·2012·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2012.07955.xPMC PMC3472042

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Abstract

Acetate supplementation increases brain acetyl‐CoA and histone acetylation and reduces lipopolysaccharide ( LPS )‐induced neuroglial activation and interleukin ( IL )‐1β expression in vivo . To determine how acetate imparts these properties, we tested the hypothesis that acetate metabolism reduces inflammatory signaling in microglia. To test this, we measured the effect acetate treatment had on cytokine expression, mitogen‐activated protein kinase ( MAPK ) signaling, histone H3 at lysine 9 acetylation, and alterations of nuclear factor‐kappa B ( NF‐κB ) in primary and BV‐2 cultured microglia. We found that treatment induced H3K9 hyperacetylation and reversed LPS‐induced H3K9 hypoacetylation similar to that found in vivo . LPS also increased IL‐1β, IL‐6, and tumor necrosis factor‐alpha ( TNF ‐α) mRNA and protein, whereas treatment returned the protein to control levels and only partially attenuated IL‐6 mRNA . In contrast, treatment increased mRNA levels of transforming growth factor‐β1 ( TGF ‐β1) and both IL‐4 mRNA and protein. LPS increased p38 MAPK and JNK phosphorylation at 4 and 2–4 h, respectively, whereas treatment reduced p38 MAPK and JNK phosphorylation only at 2 h. In addition, treatment reversed the LPS‐induced elevation of NF‐κB p65 protein and phosphorylation at serine 468 and induced acetylation at lysine 310. These data suggest that acetate metabolism reduces inflammatory signaling and alters histone and non‐histone protein acetylation.

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Authors: Soliman, M. L., Puig, K. L., Combs, C. K., & Rosenberger, T. A.
Affiliations: University of North Dakota (US)
Corresponding author: Rosenberger, Thad A.
ORCID: Combs, Colin K.
Rosenberger, Thad A.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2012-09-28
Volume: 123
Issue: 4
Pages: 555-567
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/j.1471-4159.2012.07955.x
PMC: PMC3472042
OpenAlex: W2090091665
Cited by: 131
References: 75
Citations by year: 2026: 12 · 2025: 12 · 2024: 21 · 2023: 12 · 2022: 15 · 2021: 14 · 2020: 12 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 1 · 2015: 2 · 2014: 7 · 2013: 7 · 2012: 3
FWCI: 3.06
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Center for Research Resources
component of the National Institutes of Health
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: acetate, microglia, neuroinflammation, histone H3K9 acetylation, NF-κB, MAPK signaling, p38 MAPK, JNK, lipopolysaccharide, IL-1β, acetyl-CoA, histone acetylation, non-histone protein acetylation, acetate metabolism, cytokine expression, TGF-β1
MeSH terms: Acetates, Acetylation, Analysis of Variance, Animals, Brain, Cells, Cultured, Dose-Response Relationship, Drug, Histones, L-Lactate Dehydrogenase, Lipopolysaccharides, Lysine, Mice, Inbred C57BL, Phosphorylation, RNA, Messenger, Time Factors, Signal Transduction, Cytokines, Microglia, Mitogen-Activated Protein Kinases, Mice

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Acetate reduces microglia inflammatory signaling in vitro

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