Evidence map›Paper›PMID 30067974›Full record

ArticleCell reports2018

FXR1 Is an IL-19-Responsive RNA-Binding Protein that Destabilizes Pro-inflammatory Transcripts in Vascular Smooth Muscle Cells.

Allison B Herman, Christine N Vrakas, Mitali Ray, Sheri E Kelemen, Michael J Sweredoski, Annie Moradian, Dale S Haines, Michael V Autieri

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  18. Long noncoding RNACell adhesion & migration · 2021
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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

8 authors at 2 institutions in 1 country.

Allison B HermanDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Christine N VrakasDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Mitali RayDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Sheri E KelemenDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Michael J SweredoskiProteome Exploration Laboratory, Beckman Institute, California Institute of Technology, Pasadena, CA 91125, USA.
Annie MoradianProteome Exploration Laboratory, Beckman Institute, California Institute of Technology, Pasadena, CA 91125, USA.
Dale S HainesFels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine at Temple University Philadelphia, PA 19140, USA.
Michael V AutieriDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA. Electronic address: mautieri@temple.edu.
Temple University · USCalifornia Institute of Technology · US

Funding

miRNA-mediated reduction of VSMC foam cell formationR01HL117724 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2013 to 2022
$3.8M
Attenuation of atherosclerosis by regulation of VSMC inflammatory gene mRNA stabilityR01HL141108 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2018 to 2021
$2.0M
NHLBI NIH HHS R01 HL117724NHLBI NIH HHS R01 HL141108
6 · The paper itself

Abstract

This work identifies the fragile-X-related protein (FXR1) as a reciprocal regulator of HuR target transcripts in vascular smooth muscle cells (VSMCs). FXR1 was identified as an HuR-interacting protein by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The HuR-FXR1 interaction is abrogated in RNase-treated extracts, indicating that their association is tethered by mRNAs. FXR1 expression is induced in diseased but not normal arteries. siRNA knockdown of FXR1 increases the abundance and stability of inflammatory mRNAs, while overexpression of FXR1 reduces their abundance and stability. Conditioned media from FXR1 siRNA-treated VSMCs enhance activation of naive VSMCs. RNA EMSA and RIP demonstrate that FXR1 interacts with an ARE and an element in the 3' UTR of TNFα. FXR1 expression is increased in VSMCs challenged with the anti-inflammatory cytokine IL-19, and FXR1 is required for IL-19 reduction of HuR. This suggests that FXR1 is an anti-inflammation responsive, HuR counter-regulatory protein that reduces abundance of pro-inflammatory transcripts.

Indexed as

RNA Stability3' Untranslated RegionsCells, CulturedELAV-Like Protein 1HumansInterleukinsMuscle, Smooth, VascularMyocytes, Smooth MuscleProtein BindingRNA-Binding ProteinsTumor Necrosis Factor-alpha3' Untranslated RegionsELAV-Like Protein 1FXR1 protein, humanIL19 protein, humanInterleukinsRNA-Binding ProteinsTumor Necrosis Factor-alphaanti-inflammatoryAREsAU-rich elementsFXR1HuRIL-19inflammationRNA stability

Identifiers

PMID30067974
PMCPMC11004729
OpenAlexW2885341302

What OpenQuestion holds

Textmetadata
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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.