Evidence map›Paper›PMID 30619270›Full record

ArticleFrontiers in immunology2018

Long Non-coding RNAs Are Central Regulators of the IL-1β-Induced Inflammatory Response in Normal and Idiopathic Pulmonary Lung Fibroblasts.

Marina R Hadjicharalambous, Benoit T Roux, Carol A Feghali-Bostwick, Lynne A Murray, Deborah L Clarke, Mark A Lindsay

Abstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
–field-weighted citation impact
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

50 citing papers in PubMed.

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  13. Antibody Mediated Rejection and T-cell Mediated Rejection Molecular Signatures Using Next-Generation Sequencing in Kidney Transplant Biopsies.Transplant international : official journal of the European Society for Organ Transplantation · 2024
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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

6 authors.

Marina R HadjicharalambousDepartment of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom.
Benoit T RouxDepartment of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom.
Carol A Feghali-BostwickDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Lynne A MurrayRIA IMED Biotech Unit, AstraZeneca, Gothenberg, Sweden.
Deborah L ClarkeMedImmune, Cambridge, United Kingdom.
Mark A LindsayDepartment of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom.

Funding

Resource CoreP30AR072582 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAMES C OATES · 2017 to 2026
$8.5M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
Biotechnology and Biological Sciences Research Council BB/N015630/1NIAMS NIH HHS K24 AR060297NIAMS NIH HHS P30 AR072582
6 · The paper itself

Abstract

There is accumulating evidence to indicate that long non-coding RNAs (lncRNAs) are important regulators of the inflammatory response. In this report, we have employed next generation sequencing to identify 14 lncRNAs that are differentially expressed in human lung fibroblasts following the induction of inflammation using interleukin-1β (IL-1β). Knockdown of the two most highly expressed lncRNAs, IL7AS, and MIR3142HG, showed that IL7AS negatively regulated IL-6 release whilst MIR3142HG was a positive regulator of IL-8 and CCL2 release. Parallel studies in fibroblasts derived from patients with idiopathic pulmonary fibrosis showed similar increases in IL7AS levels, that also negatively regulate IL-6 release. In contrast, IL-1β-induced MIR3142HG expression, and its metabolism to miR-146a, was reduced by 4- and 9-fold in IPF fibroblasts, respectively. This correlated with a reduced expression of inflammatory mediators whilst MIR3142HG knockdown showed no effect upon IL-8 and CCL2 release. Pharmacological studies showed that IL-1β-induced IL7AS and MIR3142HG production and release of IL-6, IL-8, and CCL2 in both control and IPF fibroblasts were mediated via an NF-κB-mediated pathway. In summary, we have cataloged those lncRNAs that are differentially expressed following IL-1β-activation of human lung fibroblasts, shown that IL7AS and MIR3142HG regulate the inflammatory response and demonstrated that the reduced inflammatory response in IPF fibroblast is correlated with attenuated expression of MIR3142HG/miR-146a.

Indexed as

Cells, CulturedChemokine CCL2FemaleFibroblastsGene Expression ProfilingGene Expression RegulationHumansIdiopathic Pulmonary FibrosisInflammationInterleukin-1betaInterleukin-6Interleukin-8MaleMiddle AgedRNA, Long NoncodingChemokine CCL2Interleukin-1betaInterleukin-6Interleukin-8RNA, Long Noncodingfibroblastfibrosisidiopathic pulmonary fibrosisinflammationinterleukin-1βlong non-coding RNAtranscriptomics

Identifiers

PMID30619270
PMCPMC6299252

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Registered trials

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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.