Evidence map›Paper›PMID 26751696›Full record

ArticlePloS one2016

Abnormal Skeletal Muscle Regeneration plus Mild Alterations in Mature Fiber Type Specification in Fktn-Deficient Dystroglycanopathy Muscular Dystrophy Mice.

Steven J Foltz, Jill N Modi, Garrett A Melick, Marin I Abousaud, Junna Luan, Marisa J Fortunato, Aaron M Beedle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Combined regenerative rehabilitation improves recovery following volumetric muscle loss injury in a rat model.Journal of biomedical materials research. Part B, Applied biomaterials · 2024
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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

7 authors at 1 institution in 1 country.

Steven J FoltzDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Jill N ModiDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Garrett A MelickDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Marin I AbousaudDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Junna LuanDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Marisa J FortunatoDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Aaron M BeedleDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
University of Georgia · US

Funding

Elucidating muscle regeneration defects in fukutin KO miceR15AR065077 · NIAMS · UNIVERSITY OF GEORGIA · PI BEEDLE, AARON M · 2014 to 2014
$390k
NIAMS NIH HHS R15 AR065077NIAMS NIH HHS R15AR065077
6 · The paper itself

Abstract

Glycosylated α-dystroglycan provides an essential link between extracellular matrix proteins, like laminin, and the cellular cytoskeleton via the dystrophin-glycoprotein complex. In secondary dystroglycanopathy muscular dystrophy, glycosylation abnormalities disrupt a complex O-mannose glycan necessary for muscle structural integrity and signaling. Fktn-deficient dystroglycanopathy mice develop moderate to severe muscular dystrophy with skeletal muscle developmental and/or regeneration defects. To gain insight into the role of glycosylated α-dystroglycan in these processes, we performed muscle fiber typing in young (2, 4 and 8 week old) and regenerated muscle. In mice with Fktn disruption during skeletal muscle specification (Myf5/Fktn KO), newly regenerated fibers (embryonic myosin heavy chain positive) peaked at 4 weeks old, while total regenerated fibers (centrally nucleated) were highest at 8 weeks old in tibialis anterior (TA) and iliopsoas, indicating peak degeneration/regeneration activity around 4 weeks of age. In contrast, mature fiber type specification at 2, 4 and 8 weeks old was relatively unchanged. Fourteen days after necrotic toxin-induced injury, there was a divergence in muscle fiber types between Myf5/Fktn KO (skeletal-muscle specific) and whole animal knockout induced with tamoxifen post-development (Tam/Fktn KO) despite equivalent time after gene deletion. Notably, Tam/Fktn KO retained higher levels of embryonic myosin heavy chain expression after injury, suggesting a delay or abnormality in differentiation programs. In mature fiber type specification post-injury, there were significant interactions between genotype and toxin parameters for type 1, 2a, and 2x fibers, and a difference between Myf5/Fktn and Tam/Fktn study groups in type 2b fibers. These data suggest that functionally glycosylated α-dystroglycan has a unique role in muscle regeneration and may influence fiber type specification post-injury.

Indexed as

RegenerationAnimalsCardiotoxinsDisease Models, AnimalDystroglycansExonsGene DeletionGenotypeGlycosylationLamininMiceMice, KnockoutMuscle Fibers, SkeletalMuscle, SkeletalMuscular Dystrophy, AnimalNecrosisCardiotoxinsDystroglycansFcmd protein, mouseLamininProteinsTransferases

Identifiers

PMID26751696
PMCPMC4708996
OpenAlexW2239699511

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.