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E-GEOD-51263

ABSTRACT: HDAC inhibition by TSA and Butyrate In Flt3L-elicited DC

OTHER RELATED OMICS DATASETS IN: PRJNA222269

PROVIDER: E-GEOD-51263 | ExpressionAtlas | 2015-07-27

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-51263-analysis-methods.tsv	Tabular
	E-GEOD-51263-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-51263-configuration.xml	Xml
	E-GEOD-51263-percentile-ranks.tsv	Tabular
	E-GEOD-51263.condensed-sdrf.tsv	Tabular

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Project description:HDAC inhibition by TSA and Butyrate In Flt3L-elicited DC

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Alternative splicing in HeLa cells after sodium butyrate treatment

Project description:We analyzed a role of histone deacetylases in alternative splicing regulation. Using human exon arrays we identified a list of 683 genes whose splicing changes after HDAC inhibition with sodium butyrate. 6 samples (3 nontreated controls and 3 sodium butyrate treated cells)

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Microbial-Derived Metabolites Regulate the Colonic Crypt Niche

Project description:In the mammalian intestine, crypts of LeiberkÃ¼hn house intestinal epithelial stem /progenitor cells at their base. We found that the presence of this structure was supported by the physiologic role of a prominent bacterial metabolite, butyrate. This bacterially-produced short chain fatty acid inhibited intestinal epithelial proliferation at physiologic concentrations. During homeostasis, butyrate did not suppress epithelial stem proliferation because it was metabolized by differentiated colonocytes. Provision of butyrate access to stem/progenitor cells either through mucosal injury or application to a crypt-less host led to inhibition of proliferation. The mechanism was dependent on HDAC inhibition in stem cells and the transcription factor Foxo3. Thus, the mammalian crypt unit structure provides energy for differentiated cells at a distance from the crypt base and this action prevents suppression of stem/progenitor proliferation. In total 4 samples were analyzed from 2 independent experiments. Two samples of colonic stem cells treated with 1mM Butyrate and two samples of colonic stem cells treated with 1mM NaCl (mock) as a control

2016-06-27 | E-GEOD-74601 | biostudies-arrayexpress

Alternative splicing in HeLa cells after sodium butyrate treatment

2011-02-03 | GSE17397 | GEO

Microbial-Derived Metabolites Regulate the Colonic Crypt Niche

Project description:In the mammalian intestine, crypts of Leiberkühn house intestinal epithelial stem /progenitor cells at their base. We found that the presence of this structure was supported by the physiologic role of a prominent bacterial metabolite, butyrate. This bacterially-produced short chain fatty acid inhibited intestinal epithelial proliferation at physiologic concentrations. During homeostasis, butyrate did not suppress epithelial stem proliferation because it was metabolized by differentiated colonocytes. Provision of butyrate access to stem/progenitor cells either through mucosal injury or application to a crypt-less host led to inhibition of proliferation. The mechanism was dependent on HDAC inhibition in stem cells and the transcription factor Foxo3. Thus, the mammalian crypt unit structure provides energy for differentiated cells at a distance from the crypt base and this action prevents suppression of stem/progenitor proliferation.

2016-06-27 | GSE74601 | GEO

HDAC inhibition by TSA and Butyrate In Flt3L-elicited DC

Project description:Butyrate induces Treg via HDACi activity Microarray of DC treated with TSA or Butyrate over untreated

2013-10-15 | E-GEOD-51263 | biostudies-arrayexpress

Effect of sodium butyrate on colorectal cancer cell line HT-29

Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.

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The Role of Butyrate as a Histone Deacetylase Inhibitor in Protecting Pancreatic Beta Cells from IL-1β-Induced Dysfunction

Project description:Butyrate, a gut microbial metabolite, has beneficial effects on glucose homeostasis and has become an attractive drug target for type 2 diabetes (T2D). Recently, we showed that butyrate protects pancreatic beta cells against cytokine-induced dysfunction. In this study, we explored the underlying mechanisms of butyrate action. Pancreatic islets were exposed to a non-cytotoxic concentration of interleukin 1β (IL-1β) for ten days to mimic the low-grade inflammation in T2D. An isoform-selective histone deacetylase 3 (HDAC3) inhibitor normalized IL-1β-reduced GSIS and insulin content similar to the effect of butyrate. In contrast, FFAR2/3 agonists failed to normalize IL-1β-induced impairment of GSIS and reduced insulin content. Butyrate, irrespective of IL-1β, inhibited HDAC activity and increased histone H3 and H4 acetylation by 3- and 10-fold, respectively. Genome-wide analysis of histone H3K27 acetylation (H3K27ac) revealed that butyrate mainly increased H3K27ac at promoter regions (~68 %), while H3K27ac peaks regulated by IL-1β were more equally distributed at promoters (~33 %), introns (~23 %) and intergenic regions (~23 %). Gene ontology analysis showed that butyrate increased IL-1β-reduced H3K27ac levels near several genes related to hormone secretion and reduced IL-1β-increased H3K27ac levels near genes associated with inflammatory responses . Butyrate alone increased H3K27ac near many genes related to MAPK signaling, hormone secretion and differentiation, and decreased H3K27ac at genes involved in cell replication. Together, these results suggest that butyrate prevents IL-1β-induced beta cell dysfunction by inhibition of HDACs resulting in changes in H3K27ac levels at genes relevant for beta cell function and inflammatory responses.

2023-12-07 | GSE233936 | GEO

An acetylation-mediated chromatin switch governs H3K4 methylation read-write capability

Project description:Cells were treated with 5mM sodium butyrate treatment (HDAC) for one hour and resulting methylation states of Lysine 4 of histone H3 were observed.

2022-03-21 | MSV000089089 | MassIVE

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