The DOI matches its Crossref record; 75 of the 75 references it cites were found in a registry or an index.
Acetate reduces microglia inflammatory signaling in vitro
Open accessAbstract
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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“acetate treatment of microglia primary culture has been shown to reduce inflammatory signaling through reduced IL-1β, IL-6, and TNF-α expression and p38 MAPK, JNK, and NF-κB phosphorylation (111).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [111]
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“acetate can be converted to acetyl-CoA, which leads to increased histone acetylation”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Soliman et al., 2012
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Cites
The language of covalent histone modifications
Strahl, B. D., & Allis, C. D. (2000) · Nature · doi:10.1038/47412 · Cited by 8,679
Mitogen-Activated Protein (MAP) Kinase Pathways: Regulation and Physiological Functions*
Pearson, G. W., Robinson, F. L., Gibson, T. B., Xu, B.-E., Karandikar, M. S., Berman, K. S., & Cobb, M. H. (2001) · Endocrine Reviews · doi:10.1210/edrv.22.2.0428 · Cited by 4,111
Microglia: Active sensor and versatile effector cells in the normal and pathologic brain
Hanisch, U.-K., & Kettenmann, H. (2007) · Nature Neuroscience · doi:10.1038/nn1997 · Cited by 3,676
Microglial physiology: unique stimuli, specialized responses
Ransohoff, R. M., & Perry, V. H. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132528 · Cited by 1,858
Acetylation and deacetylation of non-histone proteins
Glozak, M. A., Sengupta, N., Zhang, X., & Seto, E. (2005) · Gene · doi:10.1016/j.gene.2005.09.010 · Cited by 1,584
Mitogen-Activated Protein (MAP) Kinase Pathways: Regulation and Physiological Functions
Pearson, G. (2001) · Endocrine Reviews · doi:10.1210/er.22.2.153 · Cited by 1,406
Duration of Nuclear NF-κB Action Regulated by Reversible Acetylation
Chen, L., Fischle, W., Verdin, E. M., & Greene, W. C. (2001) · Science · doi:10.1126/science.1062374 · Cited by 1,231
p38 MAP kinases: key signalling molecules as therapeutic targets for inflammatory diseases
Kumar, S., Boehm, J. C., & Lee, J. C. (2003) · Nature Reviews Drug Discovery · doi:10.1038/nrd1177 · Cited by 1,199
Streit, W. J., Walter, S. A., & Pennell, N. A. (1999) · Progress in Neurobiology · doi:10.1016/s0301-0082(98)00069-0 · Cited by 1,096
Immortalization of murine microglial cells by a v-raf / v-myc carrying retrovirus
Blasi, E., Barluzzi, R., Bocchini, V., Mazzolla, R., & Bistoni, F. (1990) · Journal of Neuroimmunology · doi:10.1016/0165-5728(90)90073-v · Cited by 1,076
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The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication
Silva, Y. P., Bernardi, A., & Frozza, R. L. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00025 · Cited by 3,043
“Likewise, acetate treatment of microglia primary culture has been shown to reduce inflammatory signaling through reduced IL-1β, IL-6, and TNF-α expression and p38 MAPK, JNK, and NF-κB phosphorylation (111).”
BackgroundNey, L.-M., Wipplinger, M., Grossmann, M., Engert, N., Wegner, V. D., & Mosig, A. S. (2023) · Open Biology · doi:10.1098/rsob.230014 · Cited by 367
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Metadata
- Authors
- Soliman, M. L., Puig, K. L., Combs, C. K., & Rosenberger, T. A.
- Affiliations
- University of North Dakota (US)
- Corresponding author
- 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
- 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
- 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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