Evidence map›Paper›PMID 35363256›Full record

ArticleThe Journal of experimental medicine2022

miR-374a-5p regulates inflammatory genes and monocyte function in patients with inflammatory bowel disease.

Carlos Perez-Sanchez, Ariana Barbera Betancourt, Paul A Lyons, Zinan Zhang, Chenqu Suo, James C Lee, Eoin F McKinney, Louise K Modis, Christian Ellson, Kenneth G C Smith

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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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

10 authors at 4 institutions in 4 countries.

Carlos Perez-Sanchez *Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0002-1903-5970
Ariana Barbera Betancourt *Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0002-3381-3505
Paul A Lyons *Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0001-7035-8997
Zinan ZhangCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0003-3831-2272
Chenqu SuoCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0002-8813-0875
James C LeeCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0001-5711-9385
Eoin F McKinneyCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0003-3516-3072
Louise K ModisAdaptive Immunity Research Unit, GSK, Stevenage, UK.ORCID 0000-0003-3103-4089
Christian EllsonAdaptive Immunity Research Unit, GSK, Stevenage, UK.ORCID 0000-0003-0453-9911
Kenneth G C SmithCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0003-3829-4326
University of Cambridge · GBAge UK · GBNational Institutes of Health · USNational University of Singapore · SG

Funding

Medical Research Council MR/L019027/1Wellcome Trust
6 · The paper itself

Abstract

MicroRNAs are critical regulators of gene expression controlling cellular processes including inflammation. We explored their role in the pathogenesis of inflammatory bowel disease (IBD) and identified reduced expression of miR-374a-5p in IBD monocytes that correlated with a module of up-regulated genes related to the inflammatory response. Key proinflammatory module genes, including for example TNFα, IL1A, IL6, and OSM, were inversely correlated with miR-374a-5p and were validated in vitro. In colonic biopsies, miR-374a-5p was again reduced in expression and inversely correlated with the same inflammatory module, and its levels predicted subsequent response to anti-TNF therapy. Increased miR-374a-5p expression was shown to control macrophage-driven inflammation by suppressing proinflammatory mediators and to reduce the capacity of monocytes to migrate and activate T cells. Our findings suggest that miR-374a-5p reduction is a central driver of inflammation in IBD, and its therapeutic supplementation could reduce monocyte-driven inflammation in IBD or other immune-mediated diseases.

Indexed as

ColitisInflammatory Bowel DiseasesMicroRNAsHumansMonocytesTumor Necrosis Factor InhibitorsMicroRNAsTumor Necrosis Factor Inhibitors

Identifiers

PMID35363256
PMCPMC8980842
OpenAlexW4224120773

What OpenQuestion holds

Textmetadata
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.