Evidence map›Paper›PMID 24909122›Full record

ArticleNature communications2014

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes.

Nicholas E IIott, James A Heward, Benoit Roux, Eleni Tsitsiou, Peter S Fenwick, Luca Lenzi, Ian Goodhead, Christiane Hertz-Fowler, Andreas Heger, Neil Hall and 3 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 178 papers.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed
13.2field-weighted citation impact, top 1% 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

178 citing papers in PubMed, 291 citations in OpenAlex.

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118 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Nicholas E IIott1] CGAT Programme, MRC Functional Genomics Unit, Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford OX1 3QX, UK [2].
James A Heward1] Department of Pharmacy and Pharmacology, University of Bath, Claverton Down, BA2 7AY Bath, UK [2].
Benoit RouxDepartment of Pharmacy and Pharmacology, University of Bath, Claverton Down, BA2 7AY Bath, UK.
Eleni TsitsiouRespiratory Research Group, University Hospital of South Manchester, University of Manchester, Southmoor Road, Manchester M23 9LY, UK.
Peter S FenwickAirways Disease, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK.
Luca LenziDepartment of Functional and Comparative Genomics, Centre for Genomic Research, University of Liverpool, Liverpool L69 3BX, UK.
Ian GoodheadDepartment of Functional and Comparative Genomics, Centre for Genomic Research, University of Liverpool, Liverpool L69 3BX, UK.
Christiane Hertz-FowlerDepartment of Functional and Comparative Genomics, Centre for Genomic Research, University of Liverpool, Liverpool L69 3BX, UK.
Andreas HegerCGAT Programme, MRC Functional Genomics Unit, Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford OX1 3QX, UK.
Neil HallDepartment of Functional and Comparative Genomics, Centre for Genomic Research, University of Liverpool, Liverpool L69 3BX, UK.
Louise E DonnellyAirways Disease, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK.
David SimsCGAT Programme, MRC Functional Genomics Unit, Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford OX1 3QX, UK.
Mark A Lindsay1] Department of Pharmacy and Pharmacology, University of Bath, Claverton Down, BA2 7AY Bath, UK [2] Respiratory Research Group, University Hospital of South Manchester, University of Manchester, Southmoor Road, Manchester M23 9LY, UK [3] Airways Disease, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK.
Genomics (United Kingdom) · GBUniversity of Bath · GBImperial College London · GBUniversity of Liverpool · GBUniversity of Manchester · GB

Funding

Biotechnology and Biological Sciences Research Council BB/K006223/1Medical Research Council G0900753Medical Research Council MC_U137761446Medical Research Council MC_UU_12021/1Medical Research Council MR/K002279/1
6 · The paper itself

Abstract

Early reports indicate that long non-coding RNAs (lncRNAs) are novel regulators of biological responses. However, their role in the human innate immune response, which provides the initial defence against infection, is largely unexplored. To address this issue, here we characterize the long non-coding RNA transcriptome in primary human monocytes using RNA sequencing. We identify 76 enhancer RNAs (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide (LPS). Crucially, we demonstrate that knockdown of nuclear-localized, NF-κB-regulated, eRNAs (IL1β-eRNA) and RBT (IL1β-RBT46) surrounding the IL1β locus, attenuates LPS-induced messenger RNA transcription and release of the proinflammatory mediators, IL1β and CXCL8. We predict that lncRNAs can be important regulators of the human innate immune response.

Indexed as

Enhancer Elements, GeneticBinding SitesHumansImmunity, InnateInflammationLipopolysaccharidesMonocytesNF-kappa BPromoter Regions, GeneticRNARNA, Long NoncodingTranscription, GeneticLipopolysaccharidesNF-kappa BRNARNA, Long Noncoding

Identifiers

PMID24909122
PMCPMC4061460
OpenAlexW2167421769

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.