Evidence map›Paper›PMID 28808260›Full record

ArticleScientific reports2017

Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis.

Philip D Hamann, Benoit T Roux, James A Heward, Seth Love, Neil J McHugh, Simon W Jones, Mark A Lindsay

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Epigenetic alterations in Sjögren's syndrome patient saliva.Clinical and experimental immunology · 2020
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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 5 institutions in 1 country.

Philip D HamannDepartment of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, BA2 7AY, UK.ORCID 0000-0003-1859-5316
Benoit T RouxDepartment of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, BA2 7AY, UK.
James A HewardBarts Cancer Institute, Queen Mary University of London, London, EC1M 6BQ, UK.
Seth LoveDementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol, BS16 1LE, UK.
Neil J McHughDepartment of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, BA2 7AY, UK.
Simon W JonesMRC ARK Centre for Musculoskeletal Aging Research, University of Birmingham, Birmingham, B15 2TT, UK. s.w.jones@bham.ac.uk.
Mark A LindsayDepartment of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, BA2 7AY, UK. m.a.lindsay@bath.ac.uk.
Royal National Hospital for Rheumatic Diseases · GBUniversity of Bath · GBQueen Mary University of London · GBUniversity of Birmingham · GBUniversity of Bristol · GB

Funding

Medical Research Council MR/K00414X/1
6 · The paper itself

Abstract

Myositis is characterised by muscle inflammation and weakness. Although generally thought to be driven by a systemic autoimmune response, increasing evidence suggests that intrinsic changes in the muscle might also contribute to the pathogenesis. Long non-coding RNAs (lncRNAs) are a family of novel genes that regulate gene transcription and translation. To determine the potential role of lncRNAs, we employed next generation sequencing to examine the transcriptome in muscle biopsies obtained from two histologically distinct patient populations, inclusion body myositis (IBM) and anti-Jo-1-associated myositis (Jo-1). 1287 mRNAs and 1068 mRNAs were differentially expressed in the muscle from Jo-1 and IBM patients, respectively. Pathway analysis showed the top canonical pathway in both Jo-1 and IBM was oxidative phosphorylation and mitochondrial dysfunction. We identified 731 known and 325 novel lncRNAs in the muscles biopsies. Comparison with controls showed 55 and 46 lncRNAs were differentially expressed in IBM and Jo-1 myositis, respectively. Of these, 16 lncRNAs were differentially expressed in both IBM and Jo-1 myositis and included upregulated H19, lncMyoD and MALAT1. Given that these are known to regulate muscle proliferation and differentiation, we speculate that changes in lncRNAs might contribute to the phenotypic changes in Jo-1 and IBM myositis.

Indexed as

TranscriptomeAdultAgedAntibodies, AntinuclearHumansMiddle AgedMyositis, Inclusion BodyRNA, Long NoncodingUp-RegulationAntibodies, AntinuclearJo-1 antibodyRNA, Long Noncoding

Identifiers

PMID28808260
PMCPMC5556005
OpenAlexW2743314322

What OpenQuestion holds

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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.