Evidence map›Paper›PMID 28257760›Full record

ArticleJournal of molecular and cellular cardiology2017

Induction of MiR133a expression by IL-19 targets LDLRAP1 and reduces oxLDL uptake in VSMC.

Khatuna Gabunia, Allison B Herman, Mitali Ray, Sheri E Kelemen, Ross N England, Raul DeLa Cadena, William J Foster, Katherine J Elliott, Satoru Eguchi, Michael V Autieri

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Biomechanical signal communication in vascular smooth muscle cells.Journal of cell communication and signaling · 2020
    Review
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  14. Resolution of inflammation in immune and nonimmune cells by interleukin-19.American journal of physiology. Cell physiology · 2020
    Review
  15. Article
  16. Article
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  19. Epigenetics of metabolic syndrome.Physiological genomics · 2018
    Review
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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 1 institution in 1 country.

Khatuna GabuniaDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Allison B HermanDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Mitali RayDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Sheri E KelemenDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Ross N EnglandDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Raul DeLa CadenaDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
William J FosterDepartments of Ophthalmology & Bioengineering, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Katherine J ElliottDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Satoru EguchiDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States.
Michael V AutieriDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States. Electronic address: mautieri@temple.edu.
Temple University · 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
Mechanism of Hypertensive Vascular Remodeling and End-Organ DamageR01HL133248 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU · 2016 to 2019
$1.8M
Vascular signal as a therapeutic target for abdominal aortic aneurysmR01HL128324 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU, RIZZO, VICTOR J. · 2015 to 2018
$1.6M
Mechanisms of Th2 interleukin-driven angiogenesisR01HL115575 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL115575NHLBI NIH HHS R01 HL117724NHLBI NIH HHS R01 HL128324NHLBI NIH HHS R01 HL133248NHLBI NIH HHS R01 HL141108
6 · The paper itself

Abstract

The transformation of vascular smooth muscle cells [VSMC] into foam cells leading to increased plaque size and decreased stability is a key, yet understudied step in atherogenesis. We reported that Interleukin-19 (IL-19), a novel, anti-inflammatory cytokine, attenuates atherosclerosis by anti-inflammatory effects on VSMC. In this work we report that IL-19 induces expression of miR133a, a muscle-specific miRNA, in VSMC. Although previously unreported, we report that miR133a can target and reduce mRNA abundance, mRNA stability, and protein expression of Low Density Lipoprotein Receptor Adaptor Protein 1, (LDLRAP1), an adaptor protein which functions to internalize the LDL receptor. Mutations in this gene lead to LDL receptor malfunction and cause the Autosomal Recessive Hypercholesterolemia (ARH) disorder in humans. Herein we show that IL-19 reduces lipid accumulation in VSMC, and LDLRAP1 expression and oxLDL uptake in a miR133a-dependent mechanism. We show that LDLRAP1 is expressed in plaque and neointimal VSMC of mouse and human injured arteries. Transfection of miR133a and LDLRAP1 siRNA into VSMC reduces their proliferation and uptake of oxLDL. miR133a is significantly increased in plasma from hyperlipidemic compared with normolipidemic patients. Expression of miR133a in IL-19 stimulated VSMC represents a previously unrecognized link between vascular lipid metabolism and inflammation, and may represent a therapeutic opportunity to combat vascular inflammatory diseases.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell LineCell ProliferationCells, CulturedCholesterolEndothelial CellsGene Expression RegulationHumansHyperlipidemiasInterleukinsLipoproteins, LDLMiceMicroRNAsMyocytes, Smooth MuscleRNA InterferenceAdaptor Proteins, Signal TransducingCholesterolIL19 protein, humanInterleukinsLDLRAP1 protein, humanLipoproteins, LDLMicroRNAsMIRN133 microRNA, humanoxidized low density lipoproteinRNA, MessengerCholesterol uptakeLDLRAP1miR133aVascular smooth muscle cell

Identifiers

PMID28257760
PMCPMC5394383
OpenAlexW2594848225

What OpenQuestion holds

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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.