Evidence map›Paper›PMID 29879154›Full record

ArticlePloS one2018

Utrophin haploinsufficiency does not worsen the functional performance, resistance to eccentric contractions and force production of dystrophic mice.

Antoine Boulanger Piette, Dounia Hamoudi, Laetitia Marcadet, Frédérique Kyomi Labelle, Rares Ovidiu David, Sabrina Bossé, Anteneh Argaw, Jérôme Frenette

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 country.

Antoine Boulanger PietteCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Dounia HamoudiCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Laetitia MarcadetCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Frédérique Kyomi LabelleCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Rares Ovidiu DavidCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Sabrina BosséCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Anteneh ArgawCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Jérôme FrenetteCentre Hospitalier Universitaire de Québec, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ-CRCHUL), Université Laval, Quebec City, QC, Canada.
Centre hospitalier de l'Université Laval · CACentre hospitalier universitaire de Québec · CAUniversité Laval · CA

Funding

Canadian Institutes of Health Research JNM-123675
6 · The paper itself

Abstract

The lack of dystrophin in Duchenne muscular dystrophy (DMD) compromises the integrity and function of muscle fibers. Skeletal muscles, except the diaphragm, do not undergo progressive degeneration in adult mdx mice due to compensatory mechanisms, including structural protein upregulation. New mouse models, including utrophin haploinsufficient mdx (mdx/utrn+/-) mice, may better recapitulate DMD. Our goal was to determine whether mdx/utrn+/- worsens the mdx phenotype and to characterize the course of the disease on muscle function and contractility at 1, 2, and 5 months of age, which encompass all stages of development relevant to DMD therapy. The functional performances of mdx/utrn+/- mice showed that they are not more affected than mdx/utrn+/+ mice based on downhill treadmill running parameters and subsequent recovery measured by open-field voluntary activity. WT mice ran the entire distance (450 m) on the treadmill, with an additional 561 m during the 4 h of open-field while mdx/utrn+/+ and mdx/utrn+/- mice completed, respectively, 236 m and 273 m on the treadmill and 341 m and 287 m during the open-field period. In addition, isolated ex vivo contractile properties and repeated eccentric contractions showed that mdx/utrn+/- does not significantly worsen the function of dystrophic EDL muscles, which are mainly composed of fast-twitch fibers that are preferentially affected in DMD. Twitch, absolute tetanic, and specific tetanic forces were very similar in dystrophic EDL muscles from mdx/utrn+/+ and mdx utrn+/- mice at 1, 2, and 5 months of age. Five-month-old mdx/utrn+/+ and mdx/utrn+/- mice lost roughly 50% of their force due to repeated eccentric contractions. Thus, histological, morphological, biochemical functional and contractile observations showed that utrophin haploinsufficiency has a very limited impact on mdx mice.

Indexed as

AnimalsDisease Models, AnimalDystrophinExercise TestFemaleHaploinsufficiencyMaleMiceMice, Inbred mdxMuscle ContractionMuscle, SkeletalMuscular Dystrophy, DuchenneUtrophinDMD protein, humanDystrophinUtrn protein, mouseUtrophin

Identifiers

PMID29879154
PMCPMC5991729
OpenAlexW2807032186

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.