Evidence map›Paper›PMID 22459292›Full record

ArticleThe Journal of surgical research2012

Interleukin-5 is a potential mediator of angiotensin II-induced aneurysm formation in apolipoprotein E knockout mice.

Jun Xu, Brittney Ehrman, Linda M Graham, Matthew J Eagleton

Open access · greenAbstract read
In one paragraph

Article in The Journal of surgical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Inflammatory cell phenotypes in AAAs: their role and potential as targets for therapy.Arteriosclerosis, thrombosis, and vascular biology · 2015
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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

4 authors at 1 institution in 1 country.

Jun XuDepartment of Vascular Surgery, Cleveland Clinic Lerner College of Medicine-CWRU, Cleveland, Ohio 44195, USA.
Brittney Ehrman
Linda M Graham
Matthew J Eagleton
Cleveland Clinic Lerner College of Medicine · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Aortic Aneurysm Formation: Mechanisms of Oxidative Stress-Induced MMP ExpressionK08HL087798 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI EAGLETON, MATTHEW JEREMIAH · 2008 to 2012
$645k
NHLBI NIH HHS K08 HL087798NHLBI NIH HHS K08HL087798
6 · The paper itself

Abstract

backgroundThe aim of this study was to evaluate alterations in Th1 and Th2 cytokines during experimental abdominal aortic aneurysm (AAA) formation.

methodsAAAs were induced in apolipoprotein E null mice by infusing angiotensin II (Ang II, 1000 ng/kg/min). Aortic homogenates were assessed at 0, 7, 14, and 28 d (n = 11/time point) for select Th1 and Th2 cytokines by ELISA. Additional mice had co-administration of anti-IgG (n = 20) or anti-IL-5 (n = 20) and were assessed at 28 d for AAA. Aortic homogenates were assessed for MMP-2 and MMP-9 expression. Mouse aortic SMC (MASMC) and peritoneal-derived macrophages were treated with IL-5 (0-40 ng/mL), and cell extracts and media (0-48 h) were assessed for MMP-2 and MMP-9 expression.

resultsAng II infusion was associated with a 3.4-fold (P < 0.01) and 3.6-fold (P < 0.01) increase in IL-5 and IL-10 (respectively), and a 0.6-fold reduction in IL-6, by 7 d. Anti-IL-5, but not anti-IgG, ameliorated Ang II-induced AAA formation. Up-regulation of MMP-2 and MMP-9 was observed in aneurysmal aortas, but not in the aortas obtained from mice treated with anti-IL-5. IL-5 stimulation of MASMC increased MMP-2 and MMP-9 mRNA (2.1-fold and 2.7-fold, respectively, P < 0.01) and protein (1.6-fold and 1.9-fold, respectively, P < 0.01) by 24 h. IL-5 stimulation of macrophages did not alter MMP expression.

conclusionsAng II induces increased Th2 cytokines IL-5 and IL-10 early in the course of experimental AAA formation, and inhibition of IL-5 prevents AAA formation suggesting an important role. While IL-5 is capable of up-regulating MMP-2 and MMP-9 expression in MASMC, investigations into alternate roles in AAA formation is warranted.

Indexed as

Angiotensin IIAnimalsAortaAortic Aneurysm, AbdominalApolipoproteins ECells, CulturedInterleukin-10Interleukin-5Macrophages, PeritonealMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, KnockoutMuscle, Smooth, VascularTh1 CellsAngiotensin IIApolipoproteins EIL10 protein, mouseInterleukin-10Interleukin-5Matrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouseVasoconstrictor Agents

Identifiers

PMID22459292
PMCPMC3394914
OpenAlexW2151078385

What OpenQuestion holds

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Registered trials

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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.