Memory impairment induced by brain iron overload is accompanied by reduced H3K9 acetylation and ameliorated by sodium butyrate

Silva, P.F. da; Garcia, Vanessa Athaíde; Dornelles, Arethuza; Silva, V.K. da; Maurmann, Natasha; Portal, Bernardo Chaves Dávila; Ferreira, Rafael Dal Ponte; Piazza, Francisco Correa; Roesler, Rafaël; Schröder, Nadja

doi:10.1016/j.neuroscience.2011.10.038

Cited by 49 publications

(34 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study revealed that environmental enrichment significantly increased the levels of acetyl-H3K9 in the hippocampus and cortex of CK-p25 rats, and caused enhanced learning and memory [36]. In addition, in a model of iron-induced memory impairment, levels of H3K9 acetylation were significantly reduced in the hippocampus of rats with neonatal iron overload, but there were no changes in the acetylation levels of H3K14ac, H4K5ac, and H4K12ac [37]. A recent study has also shown that suppressed gene expression and impaired memory are related to the downregulation of histone acetylation of H3K9 and H3K14 [38].…”

Section: Discussionmentioning

confidence: 90%

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Jie

Xia

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Borna disease virus 1 (BoDV-1) infection induces cognitive impairment in rodents. Emerging evidence has demonstrated that Chromatin remodeling through histone acetylation can regulate cognitive function. In the present study, we investigated the epigenetic regulation of chromatin that underlies BoDV-1-induced cognitive changes in the hippocampus. Methods: Immunofluorescence assay was applied to detect BoDV-1 infection in hippocampal neurons and Sprague-Dawley rats models. The histone acetylation levels both in vivo and vitro were assessed by western blots. The acetylation-regulated genes were identified by ChIP-seq and verified by RT-qPCR. Cognitive functions were evaluated with Morris Water Maze test. In addition, Golgi staining, and electrophysiology were used to study changes in synaptic structure and function. Results: BoDV-1 infection of hippocampal neurons significantly decreased H3K9 histone acetylation level and inhibited transcription of several synaptic genes, including postsynaptic density 95 (PSD95) and brain-derived neurotrophic factor (BDNF). Furthermore, BoDV-1 infection of Sprague Dawley rats disrupted synaptic plasticity and caused spatial memory impairment. These rats also exhibited dysregulated hippocampal H3K9 acetylation and decreased PSD95 and BDNF protein expression. Treatment with the HDAC inhibitor, suberanilohydroxamic acid (SAHA), attenuated the negative effects of BoDV-1. Conclusion: Our results demonstrate that regulation of H3K9 histone acetylation may play an important role in BoDV-1-induced memory impairment, whereas SAHA may confer protection against BoDV-1-induced cognitive impairments. This study finds important

show abstract

Section: Discussionmentioning

confidence: 90%

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Jie

Xia

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Further, acetate increases H3K9 acetylation in astrocytes, but LPS itself does not reduce acetylated H3K9 in this cell type as found in vivo [9]. Because H3K9 acetylation is implicated in neuroinflammation and neuroglial activation [34, 55, 56], we chose to focus only on H3K9 in this study. For these reasons chromatin immunoprecipitation was performed in BV-2 microglia cultures, where H3K9 acetylation is altered by both LPS and acetate treatment.…”

Section: Discussionmentioning

confidence: 99%

Acetate Reduces PGE₂ Release and Modulates Phospholipase and Cyclooxygenase Levels in Neuroglia Stimulated with Lipopolysaccharide

Soliman

Ohm

Rosenberger

2013

Lipids

View full text Add to dashboard Cite

Acetate supplementation attenuates neuroglial activation, increases histone and non-histone protein acetylation, reduces pro-inflammatory cytokine expression, and increases IL-4 transcription in rat models of neuroinflammation and Lyme's neuroborreliosis. Because eicosanoid signaling is involved in neuroinflammation, we measured the effect acetate treatment had on phospholipase, cyclooxygenase, and prostaglandin E2 (PGE2) levels in BV-2 microglia and primary astrocytes stimulated with lipopolysaccharide (LPS). In BV-2 microglia, we found that LPS increased the phosphorylation-state of cytosolic phospholipase A2 (cPLA2), reduced the levels of phospholipase C (PLC) β1, and increased the levels of cyclooxygenase (Cox)-1 and -2. Acetate treatment returned PLCβ1 and Cox-1 levels to normal, attenuated the increase in Cox-2, but had no effect on cPLA2 phosphorylation. In primary astrocytes, LPS increased the phosphorylation of cPLA2 and increased the levels of Cox-1 and Cox-2. Acetate treatment in these cells reduced secretory PLA2 IIA and PLCβ1 levels as compared to LPS-treatment groups, reversed the increase in cPLA2 phosphorylation, and returned Cox-1 levels to normal. Acetate treatment reduced PGE2 release in astrocytes stimulated with LPS to control levels, but did not alter PGE2 levels in BV-2 microglia. The amount of acetylated H3K9 bound to the promoter regions of Cox-1, Cox-2, IL-1β and NF-κB p65 genes, but not IL-4 in were increased in BV-2 microglia treated with acetate. These data suggest that acetate treatment can disrupt eicosanoid signaling in neuroglia that may, in part, be the result of altering gene expression due chromatin remodeling as a result of increasing H3K9 acetylation.

show abstract

“…While NaB had no effect on the contextual memory on wild-type mice, contextual memory in the transgenic mouse model showed significant improvements, even at late stages of Alzheimer’s disease. These improvements in learning and memory have also been demonstrated in models of memory impairment from a toxic overload of metals [37,38], traumatic brain injury [39] or neurological infections [40,41]. …”

Section: The Functions Of Butyratementioning

confidence: 94%

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Bourassa¹,

Alim

Bultman

et al. 2016

Neuroscience Letters

468

316

View full text Add to dashboard Cite

As interest in the gut microbiome has grown in recent years, attention has turned to the impact of our diet on our brain. The benefits of a high fiber diet in the colon have been well documented in epidemiological studies, but its potential impact on the brain has largely been understudied. Here, we will review evidence that butyrate, a short-chain fatty acid (SCFA) produced by bacterial fermentation of fiber in the colon, can improve brain health. Butyrate has been extensively studied as a histone deacetylase (HDAC) inhibitor but also functions as a ligand for a subset of G protein-coupled receptors and as an energy metabolite. These diverse modes of action make it well suited for solving the wide array of imbalances frequently encountered in neurological disorders. In this review, we will integrate evidence from the disparate fields of gastroenterology and neuroscience to hypothesize that the metabolism of a high fiber diet in the gut can alter gene expression in the brain to prevent neurodegeneration and promote regeneration.

show abstract

Memory impairment induced by brain iron overload is accompanied by reduced H3K9 acetylation and ameliorated by sodium butyrate

Cited by 49 publications

References 47 publications

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Acetate Reduces PGE₂ Release and Modulates Phospholipase and Cyclooxygenase Levels in Neuroglia Stimulated with Lipopolysaccharide

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Contact Info

Product

Resources

About

Memory impairment induced by brain iron overload is accompanied by reduced H3K9 acetylation and ameliorated by sodium butyrate

Cited by 49 publications

References 47 publications

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Acetate Reduces PGE2 Release and Modulates Phospholipase and Cyclooxygenase Levels in Neuroglia Stimulated with Lipopolysaccharide

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Contact Info

Product

Resources

About

Acetate Reduces PGE₂ Release and Modulates Phospholipase and Cyclooxygenase Levels in Neuroglia Stimulated with Lipopolysaccharide