Evidence map›Paper›PMID 25610877›Full record

ArticleJournal of diabetes research2014

The class I histone deacetylase inhibitor MS-275 prevents pancreatic beta cell death induced by palmitate.

Valérie Plaisance, Laure Rolland, Valéry Gmyr, Jean-Sébastien Annicotte, Julie Kerr-Conte, François Pattou, Amar Abderrahmani

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
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

19 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Augmentation of histone deacetylase 3 (Clinical epigenetics · 2016
    Article
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

7 authors at 4 institutions in 1 country.

Valérie PlaisanceEuropean Genomic Institute for Diabetes (EGID) FR 3508, University of Lille, CNRS UMR 8199, and Faculty of Medicine West, 1 Place de Verdun, 59045 Lille, France.
Laure RollandEuropean Genomic Institute for Diabetes (EGID) FR 3508, University of Lille, CNRS UMR 8199, and Faculty of Medicine West, 1 Place de Verdun, 59045 Lille, France.
Valéry GmyrDepartment of Endocrine Surgery, Lille University Hospital, INSERM UMR 859, University of Lille, EGID FR 3508, Biotherapies for Diabetes, Lille, France.
Jean-Sébastien AnnicotteEuropean Genomic Institute for Diabetes (EGID) FR 3508, University of Lille, CNRS UMR 8199, and Faculty of Medicine West, 1 Place de Verdun, 59045 Lille, France.
Julie Kerr-ConteDepartment of Endocrine Surgery, Lille University Hospital, INSERM UMR 859, University of Lille, EGID FR 3508, Biotherapies for Diabetes, Lille, France.
François PattouDepartment of Endocrine Surgery, Lille University Hospital, INSERM UMR 859, University of Lille, EGID FR 3508, Biotherapies for Diabetes, Lille, France.
Amar AbderrahmaniEuropean Genomic Institute for Diabetes (EGID) FR 3508, University of Lille, CNRS UMR 8199, and Faculty of Medicine West, 1 Place de Verdun, 59045 Lille, France.
Centre National de la Recherche Scientifique · FREuropean Genomic Institute for Diabetes · FRUniversité de Lille · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevation of the dietary saturated fatty acid palmitate contributes to the reduction of functional beta cell mass in the pathogenesis of type 2 diabetes. The diabetogenic effect of palmitate is achieved by increasing beta cell death through induction of the endoplasmic reticulum (ER) stress markers including activating transcription factor 3 (Atf3) and CAAT/enhancer-binding protein homologous protein-10 (Chop). In this study, we investigated whether treatment of beta cells with the MS-275, a HDAC1 and HDAC3 activity inhibitor which prevents beta cell death elicited by cytokines, is beneficial for combating beta cell dysfunction caused by palmitate. We show that culture of isolated human islets and MIN6 cells with MS-275 reduced apoptosis evoked by palmitate. The protective effect of MS-275 was associated with the attenuation of the expression of Atf3 and Chop. Silencing of HDAC3, but not of HDAC1, mimicked the effects of MS-275 on the expression of the two ER stress markers and apoptosis. These data point to HDAC3 as a potential drug target for preserving beta cells against lipotoxicity in diabetes.

Indexed as

Histone DeacetylasesActivating Transcription Factor 3AnimalsApoptosisBenzamidesCell Line, TumorCytoprotectionHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHumansInsulin-Secreting CellsMicePalmitic AcidPyridinesRNA InterferenceActivating Transcription Factor 3ATF3 protein, humanAtf3 protein, mouseBenzamidesDDIT3 protein, humanDdit3 protein, mouseentinostatHDAC1 protein, humanHdac1 protein, mouseHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesPalmitic AcidPyridinesTranscription Factor CHOP

Identifiers

PMID25610877
PMCPMC4294305
OpenAlexW1983580359

What OpenQuestion holds

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Registered trials

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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.