Evidence map›Paper›PMID 24814101›Full record

ArticleThe American journal of pathology2014

IL-19 reduces ligation-mediated neointimal hyperplasia by reducing vascular smooth muscle cell activation.

Stephen Ellison, Khatuna Gabunia, James M Richards, Sheri E Kelemen, Ross N England, Dan Rudic, Yasu-Taka Azuma, M Alexandra Munroy, Satoru Eguchi, Michael V Autieri

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2014. 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
1.5field-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, 33 citations in OpenAlex.

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  15. Genetic Deletion of IL-19 (Interleukin-19) Exacerbates Atherogenesis inArteriosclerosis, thrombosis, and vascular biology · 2018
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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 3 institutions in 2 countries.

Stephen EllisonDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Khatuna GabuniaDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
James M RichardsDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Sheri E KelemenDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Ross N EnglandDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Dan RudicDepartment of Pharmacology and Toxicology, Georgia Regents University, Augusta, Georgia.
Yasu-Taka AzumaLaboratory of Veterinary Pharmacology, Osaka Prefecture University Graduate School, Osaka, Japan.
M Alexandra MunroyDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Satoru EguchiDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania.
Michael V AutieriDepartment of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania. Electronic address: mautieri@temple.edu.
Temple University · USAugusta University · USOsaka Prefecture University · JP

Funding

Integrative Cardiovascular PathophysiologyT32HL091804 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ELROD, JOHN WILLIAM · 2008 to 2024
$4.5M
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
Mechanisms of Th2 interleukin-driven angiogenesisR01HL115575 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2013 to 2016
$1.5M
Suppression of VSMC Activation and Mechanisms of Vascular Protection by IL-19R01HL090885 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2009 to 2012
$1.5M
NHLBI NIH HHS HL090885NHLBI NIH HHS HL115575NHLBI NIH HHS R01 HL090885NHLBI NIH HHS R01 HL115575NHLBI NIH HHS R01 HL117724NHLBI NIH HHS R01 HL141108NHLBI NIH HHS T32 HL091804
6 · The paper itself

Abstract

We tested the hypothesis that IL-19, a putative member of the type 2 helper T-cell family of anti-inflammatory interleukins, can attenuate intimal hyperplasia and modulate the vascular smooth muscle cell (VSMC) response to injury. Ligated carotid artery of IL-19 knockout (KO) mice demonstrated a significantly higher neointima/intima ratio compared with wild-type (WT) mice (P = 0.04). More important, the increased neointima/intima ratio in the KO could be reversed by injection of 10 ng/g per day recombinant IL-19 into the KO mouse (P = 0.04). VSMCs explanted from IL-19 KO mice proliferated significantly more rapidly than WT. This could be inhibited by addition of IL-19 to KO VSMCs (P = 0.04 and P < 0.01). IL-19 KO VSMCs migrated more rapidly compared with WT (P < 0.01). Interestingly, there was no type 1 helper T-cell polarization in the KO mouse, but there was significantly greater leukocyte infiltrate in the ligated artery in these mice compared with WT. IL-19 KO VSMCs expressed significantly greater levels of inflammatory mRNA, including IL-1β, tumor necrosis factor α, and monocyte chemoattractant protein-1 in response to tumor necrosis factor α stimulation (P < 0.01 for all). KO VSMCs expressed greater adhesion molecule expression and adherence to monocytes. Together, these data indicate that IL-19 is a previously unrecognized counterregulatory factor for VSMCs, and its expression is an important protective mechanism in regulation of vascular restenosis.

Indexed as

AnimalsCell MovementCell ProliferationCells, CulturedFemaleHyperplasiaInterleukin-10InterleukinsLigationMaleMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaRecombinant ProteinsIl19 protein, mouseInterleukin-10InterleukinsRecombinant Proteins

Identifiers

PMID24814101
PMCPMC4076471
OpenAlexW1985643407

What OpenQuestion holds

Textmetadata
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.