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

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...

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Autores principales:	Philip D. Hamann, Benoit T. Roux, James A. Heward, Seth Love, Neil J. McHugh, Simon W. Jones, Mark A. Lindsay
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5400111e740e4193ae72b381e078af27
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spelling	oai:doaj.org-article:5400111e740e4193ae72b381e078af272021-12-02T15:05:06ZTranscriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis10.1038/s41598-017-08603-92045-2322https://doaj.org/article/5400111e740e4193ae72b381e078af272017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08603-9https://doaj.org/toc/2045-2322Abstract 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.Philip D. HamannBenoit T. RouxJames A. HewardSeth LoveNeil J. McHughSimon W. JonesMark A. LindsayNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Philip D. Hamann Benoit T. Roux James A. Heward Seth Love Neil J. McHugh Simon W. Jones Mark A. Lindsay Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
description	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.
format	article
author	Philip D. Hamann Benoit T. Roux James A. Heward Seth Love Neil J. McHugh Simon W. Jones Mark A. Lindsay
author_facet	Philip D. Hamann Benoit T. Roux James A. Heward Seth Love Neil J. McHugh Simon W. Jones Mark A. Lindsay
author_sort	Philip D. Hamann
title	Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
title_short	Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
title_full	Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
title_fullStr	Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
title_full_unstemmed	Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis
title_sort	transcriptional profiling identifies differential expression of long non-coding rnas in jo-1 associated and inclusion body myositis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/5400111e740e4193ae72b381e078af27
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Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis

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