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Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome (ChIP-Seq)

ABSTRACT: ChIP-Seq analysis revealed that suberoylanilidehydroxamic acid (SAHA) increases genome-wide H4 acetylation in differentially regulated genes, except for the 500 bp upstream of transcription start sites (TSS).

ORGANISM(S): Mus musculus

PROVIDER: GSE50551 | GEO | 2013/09/04

SECONDARY ACCESSION(S): PRJNA217926

REPOSITORIES: GEO

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Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome (ChIP-Seq)

Project description:ChIP-Seq analysis revealed that suberoylanilidehydroxamic acid (SAHA) increases genome-wide H4 acetylation in differentially regulated genes, except for the 500 bp upstream of transcription start sites (TSS). Chromatin immunoprecipitation (ChIP) with massively parallel high throughput sequencing (Seq) was used to map genome-wide histone H4 acetylation (K4/7/11/15) in the presence or absence of SAHA in differentiating MC3T3 sc4 osteoblasts.

2013-09-04 | E-GEOD-50551 | biostudies-arrayexpress

Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome (BeadChip)

Project description:Suberoylanilidehydroxamic acid (SAHA) significantly increased the expression levels of 127 transcripts and suppressed expression of 130 genes by more than 2-fold within 3 standard deviations of the mean in differentiating MC3T3 sc4 osteoblasts Total RNA was obtained from differentiating MC3T3 sc4 cells treated with SAHA or vehicle (DMSO).

2013-09-04 | E-GEOD-50549 | biostudies-arrayexpress

Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome (BeadChip)

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Histone deacetylase inhibition promotes osteoblast maturation by altering the histone H4 epigenome and reduces Akt phosphorylation.

Project description:Bone has remarkable regenerative capacity, but this ability diminishes during aging. Histone deacetylase inhibitors (HDIs) promote terminal osteoblast differentiation and extracellular matrix production in culture. The epigenetic events altered by HDIs in osteoblasts may hold clues for the development of new anabolic treatments for osteoporosis and other conditions of low bone mass. To assess how HDIs affect the epigenome of committed osteoblasts, MC3T3 cells were treated with suberoylanilide hydroxamic acid (SAHA) and subjected to microarray gene expression profiling and high-throughput ChIP-Seq analysis. As expected, SAHA induced differentiation and matrix calcification of osteoblasts in vitro. ChIP-Seq analysis revealed that SAHA increased histone H4 acetylation genome-wide and in differentially regulated genes, except for the 500 bp upstream of transcriptional start sites. Pathway analysis indicated that SAHA increased the expression of insulin signaling modulators, including Slc9a3r1. SAHA decreased phosphorylation of insulin receptor ?, Akt, and the Akt substrate FoxO1, resulting in FoxO1 stabilization. Thus, SAHA induces genome-wide H4 acetylation and modulates the insulin/Akt/FoxO1 signaling axis, whereas it promotes terminal osteoblast differentiation in vitro.

| S-EPMC3789974 | biostudies-literature

Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-09-04 | E-GEOD-50552 | biostudies-arrayexpress

Histone Deacetylase Inhibition Promotes Osteoblast Maturation by Altering the Histone 4 (H4) Epigenome

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-09-04 | GSE50552 | GEO

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Project description:We performed a high-throughput mapping of the 5’ end transcriptome of the pAA plasmid of the clinical Escherichia coli O104:H4 (E. coli O104:H4) isolate LB226692. We employed differential RNA-sequencing (dRNA-seq), a terminator exonuclease (TEX)-based RNA-seq approach allowing for the discrimination of primary and processed transcripts. This method has proven to be a powerful tool for the mapping of transcription start sites (TSS) and detection of non-coding RNAs (ncRNAs) in bacteria. We catalogued pAA-associated TSS and processing sites on a plasmid-wide scale and performed a detailed analysis of the primary transcriptome focusing on pAA virulence gene expression.

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Top Down Histone H4 - SUM159 Butyrate

Project description:Proteins physiologically exist and function as ‘proteoforms’ that arise from one gene but acquire additional function by further variation such as post-translational modification (PTM). When multiple PTMs coexist on single protein molecules top down proteomics becomes the only feasible method; however, most top down methods have limited quantitative capacity and insufficient throughput to truly address proteoform biology. Here we demonstrate that, with meticulous design and diligent consideration of statistics, top down proteomics is quantitative, reproducible, sensitive, and high throughput. The proteoforms of histone H4 are well-studied both as a challenging proteoform identification problem and due to their essential role in the regulation of all eukaryotic DNA templated processes, including gene expression. Much of histone H4’s function is obfuscated from prevailing methods due to combinatorial mechanisms. Starting from cells or tissues, after an optimized protein purification process the H4 proteoforms are physically separated by online C-3 chromatography, narrowly isolated in MS1 and sequenced with ETD fragmentation. With this method we achieve more than 30 replicates from a single 35mm tissue culture dish by loading 55ng of H4 on column. Parallelization and automation yield a sustained throughput of 12 replicates per day, operating continuously for weeks. We achieve reproducible quantitation (average biological Pearson correlations of 0.89) of hundreds of proteoforms (about 200-300) over almost six orders of magnitude and an estimated LLoQ of 0.001% abundance. We demonstrate the capacity of the method to precisely measure well-established changes with sodium butyrate treatment of SUM159 cells.

2019-11-22 | PXD013766 | Pride

Targeting the epigenome: Screening bioactive compounds that regulate histone deacetylase activity.

Project description:Nutrigenomics is a rapidly expanding field that elucidates the link between diet-genome interactions. Recent evidence demonstrates that regulation of the epigenome, and in particular inhibition of histone deacetylases (HDACs), impact pathogenetic mechanisms involved in chronic disease. Few studies, to date, have screened libraries of bioactive compounds that act as epigenetic modifiers. This study screened a library of 131 natural compounds to determine bioactive compounds that inhibit Zn-dependent HDAC activity.Using class-specific HDAC substrates, we screened 131 natural compounds for HDAC activity in bovine cardiac tissue. From this screen, we identified 18 bioactive compound HDAC inhibitors. Using our class-specific HDAC substrates, we next screened these 18 bioactive compounds against recombinant HDAC proteins. Consistent with inhibition of HDAC activity, these compounds were capable of inhibiting activity of individual HDAC isoforms. Lastly, we report that treatment of H9c2 cardiac myoblasts with bioactive HDAC inhibitors was sufficient to increase lysine acetylation as assessed via immunoblot.This study provided the first step in identifying multiple bioactive compound HDAC inhibitors. Taken together, this report sets the stage for future exploration of these bioactive compounds as epigenetic regulators to potentially ameliorate chronic disease.

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