Evidence map›Paper›PMID 26860865›Full record

ArticleHistochemistry and cell biology2016

Facioscapulohumeral dystrophy myoblasts efficiently repair moderate levels of oxidative DNA damage.

Yara Bou Saada, Carla Dib, Petr Dmitriev, Aline Hamade, Gilles Carnac, Dalila Laoudj-Chenivesse, Marc Lipinski, Yegor S Vassetzky

Abstract read
PubMed Publisher
In one paragraph

Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  16. In focus in Vienna: the cell nucleus.Histochemistry and cell biology · 2016
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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

8 authors at 3 institutions in 3 countries.

Yara Bou SaadaUMR 8126, CNRS, Univ. Paris-Sud, Institut de Cancérologie Gustave-Roussy, Université Paris Saclay, 94805, Villejuif, France.
Carla DibUMR 8126, CNRS, Univ. Paris-Sud, Institut de Cancérologie Gustave-Roussy, Université Paris Saclay, 94805, Villejuif, France.
Petr DmitrievUMR 8126, CNRS, Univ. Paris-Sud, Institut de Cancérologie Gustave-Roussy, Université Paris Saclay, 94805, Villejuif, France.
Aline HamadeER030-EDST, Department of Life and Earth Sciences, Faculty of Sciences II, Lebanese University, Beirut, Lebanon.
Gilles CarnacINSERM U-1046, 371 Avenue du Doyen Gaston Giraud, 34295, Montpellier, France.
Dalila Laoudj-ChenivesseINSERM U-1046, 371 Avenue du Doyen Gaston Giraud, 34295, Montpellier, France.
Marc LipinskiUMR 8126, CNRS, Univ. Paris-Sud, Institut de Cancérologie Gustave-Roussy, Université Paris Saclay, 94805, Villejuif, France.
Yegor S VassetzkyUMR 8126, CNRS, Univ. Paris-Sud, Institut de Cancérologie Gustave-Roussy, Université Paris Saclay, 94805, Villejuif, France. vassetzky@igr.fr.ORCID http://orcid.org/0000-0003-3101-7043
Université Paris-Sud · FRInserm · FRLebanese University · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Facioscapulohumeral dystrophy (FSHD) is a progressive muscular dystrophy linked to a deletion of a subset of D4Z4 macrosatellite repeats accompanied by a chromatin relaxation of the D4Z4 array on chromosome 4q. In vitro, FSHD primary myoblasts show altered expression of oxidative-related genes and are more susceptible to oxidative stress. Double homeobox 4 (DUX4) gene, encoded within each D4Z4 unit, is normally transcriptionally silenced but is found aberrantly expressed in skeletal muscles of FSHD patients. Its expression leads to a deregulation of DUX4 target genes including those implicated in redox balance. Here, we assessed DNA repair efficiency of oxidative DNA damage in FSHD myoblasts and DUX4-transfected myoblasts. We have shown that the DNA repair activity is altered neither in FSHD myoblasts nor in immortalized human myoblasts transiently expressing DUX4. DNA damage caused by moderate doses of an oxidant is efficiently repaired while FSHD myoblasts exposed for 24 h to high levels of oxidative stress accumulated more DNA damage than normal myoblasts, suggesting that FSHD myoblasts remain more vulnerable to oxidative stress at high doses of oxidants.

Indexed as

DNA DamageDNA RepairOxidative StressCells, CulturedHomeodomain ProteinsHumansHydrogen PeroxideMuscular Dystrophy, FacioscapulohumeralMyoblasts, SkeletalDUX4L1 protein, humanHomeodomain ProteinsHydrogen PeroxideDNA damageDNA repairDUX4Facioscapulohumeral dystrophyOxidative stress

Identifiers

PMID26860865
OpenAlexW2273534944

What OpenQuestion holds

Textmetadata
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.