Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis.
Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis.
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DOI：
10.1038/s41598-017-08603-9
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发表时间：
2017-08-14
影响因子：
4.6
通讯作者：
Lindsay MA
中科院分区：
文献类型：
--
作者：
Hamann PD;Roux BT;Heward JA;Love S;McHugh NJ;Jones SW;Lindsay MA
肌炎的特征是肌肉发炎和无力。虽然通常认为是由全身性自身免疫反应驱动，但越来越多的证据表明，肌肉的内在变化也可能导致发病机制。长链非编码RNA（longnon-codingRNA，lncRNA）是一类调控基因转录和翻译的新基因。为了确定lncRNA的潜在作用，我们采用下一代测序来检查从两个组织学上不同的患者群体（包涵体肌炎（IBM）和抗Jo-1相关肌炎（Jo-1））获得的肌肉活检中的转录组。Jo-1和IBM患者肌肉中分别有1287和1068个mRNA差异表达。通路分析显示，在Jo-1和IBM中，最重要的经典通路是氧化磷酸化和线粒体功能障碍。我们在肌肉活检中鉴定了731个已知的和325个新的lncRNA。与对照组相比，IBM和Jo-1肌炎中分别有55和46个lncRNA差异表达。其中，16个lncRNA在IBM和Jo-1肌炎中差异表达，包括上调的H19、lncMyoD和MALAT 1。鉴于这些已知调节肌肉增殖和分化，我们推测lncRNA的变化可能有助于Jo-1和IBM肌炎的表型变化。
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.
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DOI：
10.1002/art.39520
发表时间：
2016-04
期刊：
Arthritis & rheumatology (Hoboken, N.J.)
影响因子：
--
作者：
Pearson MJ;Philp AM;Heward JA;Roux BT;Walsh DA;Davis ET;Lindsay MA;Jones SW
通讯作者：
Jones SW
DOI：
10.1093/bioinformatics/btq033
发表时间：
2010-03-15
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Quinlan AR;Hall IM
通讯作者：
Hall IM
DOI：
10.1126/science.aah7111
发表时间：
2017-01-06
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Liu SJ;Horlbeck MA;Cho SW;Birk HS;Malatesta M;He D;Attenello FJ;Villalta JE;Cho MY;Chen Y;Mandegar MA;Olvera MP;Gilbert LA;Conklin BR;Chang HY;Weissman JS;Lim DA
通讯作者：
Lim DA
影响因子：
6
作者：
Ivanidze, Jana;Hoffmann, Reinhard;Dornmair, Klaus
通讯作者：
Dornmair, Klaus
影响因子：
10.5
作者：
Cabili, Moran N.;Trapnell, Cole;Rinn, John L.
通讯作者：
Rinn, John L.