Evidence map›Paper›PMID 24732587›Full record

ArticleGenome research2014

Vascular histone deacetylation by pharmacological HDAC inhibition.

Haloom Rafehi, Aneta Balcerczyk, Sebastian Lunke, Antony Kaspi, Mark Ziemann, Harikrishnan Kn, Jun Okabe, Ishant Khurana, Jenny Ooi, Abdul Waheed Khan and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 91 citations in OpenAlex.

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  12. Inhibition of pancreatic EZH2 restores progenitor insulin in T1D donor.Signal transduction and targeted therapy · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Haloom RafehiBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia;
Aneta BalcerczykBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Sebastian LunkeBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Antony KaspiBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Mark ZiemannBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Harikrishnan KnBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Jun OkabeBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Faculty of Medicine, Monash University, Victoria 3800, Australia.
Ishant KhuranaBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Jenny OoiBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Abdul Waheed KhanBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Xiao-Jun DuBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Faculty of Medicine, Monash University, Victoria 3800, Australia assam.el-osta@bakeridi.edu.au.
Lisa ChangBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Izhak HavivBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Samuel T KeatingBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Tom C KaragiannisBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia;
Assam El-OstaBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia; Faculty of Medicine, Monash University, Victoria 3800, Australia assam.el-osta@bakeridi.edu.au.
Baker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HDAC inhibitors can regulate gene expression by post-translational modification of histone as well as nonhistone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action. However, little is known of the extent of genome-wide changes in cells stimulated by the hydroxamic acids, TSA and SAHA. In this article, we map vascular chromatin modifications including histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation-mediated gene expression is often associated with modification of other lysine residues, we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). RNA sequencing indicates the differential expression of ∼30% of genes, with almost equal numbers being up- and down-regulated. We observed broad deacetylation and gene expression changes conferred by TSA and SAHA mediated by the loss of EP300/CREBBP binding at multiple gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation by pharmacological HDAC inhibition.

Indexed as

AcetylationAnimalsAnti-Inflammatory AgentsAortaCells, CulturedEndothelial CellsEndothelium, VascularGene Expression RegulationGenome, HumanHistone Deacetylase InhibitorsHistonesHumansHydroxamic AcidsMaleMice, Inbred C57BLPromoter Regions, GeneticAnti-Inflammatory AgentsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsTranscription Factorstrichostatin AVorinostat

Identifiers

PMID24732587
PMCPMC4120081
OpenAlexW2128980492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.