Evidence map›Paper›PMID 27922090›Full record

ArticleScientific reports2016

miR-146a-mediated suppression of the inflammatory response in human adipocytes.

Julian Roos, Eveliina Enlund, Jan-Bernd Funcke, Daniel Tews, Karlheinz Holzmann, Klaus-Michael Debatin, Martin Wabitsch, Pamela Fischer-Posovszky

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

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

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

8 authors at 2 institutions in 1 country.

Julian RoosDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Eveliina EnlundDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Jan-Bernd FunckeDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Daniel TewsDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Karlheinz HolzmannCore Facility Genomics, Ulm University, Ulm, Germany.
Klaus-Michael DebatinDepartment of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Martin WabitschDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Pamela Fischer-PosovszkyDivision of Pediatric Endocrinology and Diabetes, Department of Pediatric and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Universität Ulm · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The obesity-associated inflammation of white adipose tissue (WAT) is one of the factors leading to the development of related diseases such as insulin resistance and liver steatosis. Recently, microRNAs (miRNAs) were identified as important regulators of WAT functions. Herein, we cultured human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes with macrophage-conditioned medium (MacCM) and performed an Affimetrix miRNA array to identify miRNAs differentially expressed under inflammatory conditions. We identified 24 miRNAs differentially expressed upon inflammation in human adipocytes and miR-146a was the most up-regulated miRNA species. In subcutaneous WAT, miR-146a was elevated in both human and murine obesity. Transfection of miR-146a mimics prevented the MacCM-induced inflammatory response in SGBS adipocytes as seen by reduced levels of IL-8 and MCP-1 mRNA and protein. We identified IRAK1 and TRAF6 as targets of miR-146a in human adipocytes and detected a reduced inflammation-induced activation of JNK and p38 upon miR-146a transfection. Taken together, we could show that miR-146a reduces the inflammatory response in human adipocytes. In a negative feedback loop miR-146a might contribute to the regulation of inflammatory processes in WAT and possibly prevent an overwhelming inflammatory response.

Indexed as

Adipocytes, WhiteAdipose Tissue, WhiteArrhythmias, CardiacChemokine CCL2Culture Media, ConditionedFeedback, PhysiologicalFemaleGene Expression RegulationGenetic Diseases, X-LinkedGigantismHeart Defects, CongenitalHumansInflammationIntellectual DisabilityInterleukin-1 Receptor-Associated KinasesInterleukin-8CCL2 protein, humanChemokine CCL2Culture Media, ConditionedInterleukin-1 Receptor-Associated KinasesInterleukin-8Intracellular Signaling Peptides and ProteinsIRAK1 protein, humanMAP Kinase Kinase 4MicroRNAsMIRN146 microRNA, humanOligoribonucleotidesp38 Mitogen-Activated Protein KinasesRNA, Small InterferingTifab protein, humanTNF Receptor-Associated Factor 6

Identifiers

PMID27922090
PMCPMC5138634
OpenAlexW2172688163

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.