Evidence map›Paper›PMID 29554127›Full record

ArticlePloS one2018

Expression profiling of disease progression in canine model of Duchenne muscular dystrophy.

Candice Brinkmeyer-Langford, Candice Chu, Cynthia Balog-Alvarez, Xue Yu, James J Cai, Mary Nabity, Joe N Kornegay

Erratum issuedOpen 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. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  14. Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Candice Brinkmeyer-LangfordDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States of America.ORCID 0000-0001-6423-8585
Candice ChuDepartment of Veterinary Pathobiology, Texas A&M University, College Station, TX, United States of America.
Cynthia Balog-AlvarezDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States of America.
Xue YuDepartment of Veterinary Pathobiology, Texas A&M University, College Station, TX, United States of America.
James J CaiDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States of America.
Mary NabityDepartment of Veterinary Pathobiology, Texas A&M University, College Station, TX, United States of America.
Joe N KornegayDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States of America.
Texas A&M University · US

Funding

MADS-box transcriptional regulation of dimorphic transition in Penicillium marneffeiR21AI126219 · NIAID · TEXAS A&M AGRILIFE RESEARCH · PI CAI, JAMES JING, LIN, XIAORONG · 2016 to 2017
$383k
NIAID NIH HHS R21 AI126219
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) causes progressive disability in 1 of every 5,000 boys due to the lack of functional dystrophin protein. Despite much advancement in knowledge about DMD disease presentation and progression-attributable in part to studies using mouse and canine models of the disease-current DMD treatments are not equally effective in all patients. There remains, therefore, a need for translational animal models in which novel treatment targets can be identified and evaluated. Golden Retriever muscular dystrophy (GRMD) is a phenotypically and genetically homologous animal model of DMD. As with DMD, speed of disease progression in GRMD varies substantially. However, unlike DMD, all GRMD dogs possess the same causal mutation; therefore genetic modifiers of phenotypic variation are relatively easier to identify. Furthermore, the GRMD dogs used in this study reside within the same colony, reducing the confounding effects of environment on phenotypic variation. To detect modifiers of disease progression, we developed gene expression profiles using RNA sequencing for 9 dogs: 6 GRMD dogs (3 with faster-progressing and 3 with slower-progressing disease, based on quantitative, objective biomarkers) and 3 control dogs from the same colony. All dogs were evaluated at 2 time points: early disease onset (3 months of age) and the point at which GRMD stabilizes (6 months of age) using quantitative, objective biomarkers identified as robust against the effects of relatedness/inbreeding. Across all comparisons, the most differentially expressed genes fell into 3 categories: myogenesis/muscle regeneration, metabolism, and inflammation. Our findings are largely in concordance with DMD and mouse model studies, reinforcing the utility of GRMD as a translational model. Novel findings include the strong up-regulation of chitinase 3-like 1 (CHI3L1) in faster-progressing GRMD dogs, suggesting previously unexplored mechanisms underlie progression speed in GRMD and DMD. In summary, our findings support the utility of RNA sequencing for evaluating potential biomarkers of GRMD progression speed, and are valuable for identifying new avenues of exploration in DMD research.

Indexed as

Gene Expression ProfilingGene Expression RegulationAnimalsBiomarkersDisease Models, AnimalDogsHumansMiceMuscle ProteinsMuscular Dystrophy, DuchenneBiomarkersMuscle Proteins

Identifiers

PMID29554127
PMCPMC5858769
OpenAlexW2793055738

What OpenQuestion 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 OpenQuestion graph.