Evidence map›Paper›PMID 26321630›Full record

ArticleCell reports2015

TNF-α-Induced microRNAs Control Dystrophin Expression in Becker Muscular Dystrophy.

Alyson A Fiorillo, Christopher R Heier, James S Novak, Christopher B Tully, Kristy J Brown, Kitipong Uaesoontrachoon, Maria C Vila, Peter P Ngheim, Luca Bello, Joe N Kornegay and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 83 citations in OpenAlex.

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  19. Therapeutic approaches for Duchenne muscular dystrophy.Nature reviews. Drug discovery · 2023
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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

14 authors at 4 institutions in 2 countries.

Alyson A FiorilloCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Christopher R HeierCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
James S NovakCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Christopher B TullyCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Kristy J BrownCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA; Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC 20010, USA.
Kitipong UaesoontrachoonCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Maria C VilaCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Peter P NgheimCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA.
Luca BelloCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA; Fondazione Ospedale S. Camillo, IRCCS, Lido Venice 30126, Italy.
Joe N KornegayDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX 77845, USA.
Corrado AngeliniFondazione Ospedale S. Camillo, IRCCS, Lido Venice 30126, Italy.
Terence A PartridgeCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA; Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC 20010, USA.
Kanneboyina NagarajuCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA; Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC 20010, USA.
Eric P HoffmanCenter for Genetic Medicine Research, Children's National Medical Center, Washington, DC 20010, USA; Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC 20010, USA. Electronic address: ehoffman@childrensnational.org.
Children's National · USGeorge Washington University · USOspedale generale di zona San Camillo Treviso · ITTexas A&M University · US

Funding

RNA fidelity and protein function of Becker-like in-frame deletionsP50AR060836 · NIAMS · CHILDREN'S RESEARCH INSTITUTE · PI HOFFMAN, ERIC P. · 2011 to 2015
$7.8M
Improved Diagnostic of the Muscular DystrophiesR01NS029525 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HOFFMAN, ERIC P. · 1991 to 2015
$6.5M
Preclinical dosing optimization: Dosing schedule, tissueU54HD071601 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI JOSE, PEDRO A. · 2011 to 2015
$4.0M
Genetics and Genomics of Muscle Postdoctoral Training ProgramT32AR056993 · NIAMS · CHILDREN'S RESEARCH INSTITUTE · PI JAISWAL, JYOTI K, PARTRIDGE, TERENCE A · 2010 to 2019
$2.2M
Mechanisms of anti-inflammation and membrane stabilization in muscular dystrophyR00HL130035 · NHLBI · CHILDREN'S RESEARCH INSTITUTE · PI HEIER, CHRISTOPHER RYAN · 2017 to 2019
$730k
Mechanisms of anti-inflammation and membrane stabilization in muscular dystrophyK99HL130035 · NHLBI · CHILDREN'S RESEARCH INSTITUTE · PI HEIER, CHRISTOPHER RYAN · 2015 to 2016
$191k
NHLBI NIH HHS K99 HL130035NHLBI NIH HHS K99HL130035NHLBI NIH HHS R00 HL130035NIAMS NIH HHS 1P50AR060836-01NIAMS NIH HHS 5T32AR056993NIAMS NIH HHS L40 AR068727NIAMS NIH HHS P50 AR060836NIAMS NIH HHS T32 AR056993NICHD NIH HHS 1U54HD071601-01NICHD NIH HHS U54 HD071601NINDS NIH HHS R01 NS029525Telethon GTB12001
6 · The paper itself

Abstract

The amount and distribution of dystrophin protein in myofibers and muscle is highly variable in Becker muscular dystrophy and in exon-skipping trials for Duchenne muscular dystrophy. Here, we investigate a molecular basis for this variability. In muscle from Becker patients sharing the same exon 45-47 in-frame deletion, dystrophin levels negatively correlate with microRNAs predicted to target dystrophin. Seven microRNAs inhibit dystrophin expression in vitro, and three are validated in vivo (miR-146b/miR-374a/miR-31). microRNAs are expressed in dystrophic myofibers and increase with age and disease severity. In exon-skipping-treated mdx mice, microRNAs are significantly higher in muscles with low dystrophin rescue. TNF-α increases microRNA levels in vitro whereas NFκB inhibition blocks this in vitro and in vivo. Collectively, these data show that microRNAs contribute to variable dystrophin levels in muscular dystrophy. Our findings suggest a model where chronic inflammation in distinct microenvironments induces pathological microRNAs, initiating a self-sustaining feedback loop that exacerbates disease progression.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceBinding SitesDogsDystrophinGene ExpressionHumansMice, Inbred C57BLMicroRNAsMuscle, SkeletalMuscular Dystrophy, DuchenneRNA InterferenceTranscriptional ActivationTumor Necrosis Factor-alpha3' Untranslated RegionsDystrophinMicroRNAsTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID26321630
PMCPMC4757433
OpenAlexW1622083158

What OpenQuestion holds

Textmetadata
LicenceTDM
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.