Evidence map›Paper›PMID 21278304›Full record

ArticleAmerican journal of respiratory and critical care medicine2011

RIG-like helicase innate immunity inhibits vascular endothelial growth factor tissue responses via a type I IFN-dependent mechanism.

Bing Ma, Charles S Dela Cruz, Dominik Hartl, Min-Jong Kang, Shervin Takyar, Robert J Homer, Chun Geun Lee, Jack A Elias

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2011. 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
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

15 citing papers in PubMed, 38 citations in OpenAlex.

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  14. Role of IL-18 in second-hand smoke-induced emphysema.American journal of respiratory cell and molecular biology · 2013
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Bing MaSection of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
Charles S Dela Cruz
Dominik Hartl
Min-Jong Kang
Shervin Takyar
Robert J Homer
Chun Geun Lee
Jack A Elias
Yale University · USPulmonary and Critical Care Associates · US

Funding

Preotease/Cathepsin-Mediated Apoptosis in COPDR01HL079328 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2005 to 2012
$3.2M
VEGF in Th2 Inflammation and AsthmaR01HL078744 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2004 to 2008
$2.0M
Molecular and Cellular Interactions Between Cigarette Smoke Exposure and RSV K08HL103770 · NHLBI · YALE UNIVERSITY · PI DELA CRUZ, CHARLES S · 2010 to 2014
$670k
NHLBI NIH HHS HL-078744NHLBI NIH HHS HL-079328NHLBI NIH HHS K08 HL103770
6 · The paper itself

Abstract

rationaleVascular endothelial growth factor (VEGF) regulates vascular, inflammatory, remodeling, and cell death responses. It plays a critical role in normal pulmonary physiology, and VEGF excess and deficiency have been implicated in the pathogenesis of asthma and chronic obstructive pulmonary disease, respectively. Although viruses are an important cause of chronic obstructive pulmonary disease exacerbations and innate responses play an important role in these exacerbations, the effects of antiviral responses on VEGF homeostasis have not been evaluated.

objectivesWe hypothesized that antiviral innate immunity regulates VEGF tissue responses.

methodsWe compared the effects of transgenic VEGF(165) in mice treated with viral pathogen-associated molecular pattern polyinosinic:polycytidylic acid [poly(I:C)], mice treated with live virus, and control mice. MEASUREMENTS AND MAIN

resultsTransgenic VEGF stimulated angiogenesis, edema, inflammation, and mucin accumulation. Each of these was abrogated by poly(I:C). These inhibitory effects were dose dependent, noted when poly(I:C) was administered before and after transgene activation, and mediated by a Toll-like receptor-3-independent and RIG-like helicase (RLH)- and type I IFN receptor-dependent pathway. VEGF stimulated the expression of VEGF receptor-1 and poly(I:C) inhibited this stimulation. Poly(I:C) also inhibited the ability of VEGF to activate extracellular signal-regulated kinase-1, Akt, focal adhesion kinase, and endothelial nitric oxide synthase, and aeroallergen-induced adaptive helper T-cell type 2 inflammation. Influenza and respiratory syncytial virus also inhibited VEGF-induced angiogenesis.

conclusionsThese studies demonstrate that poly(I:C) and respiratory viruses inhibit VEGF-induced tissue responses and adaptive helper T-cell type 2 inflammation and highlight the importance of a RLH- and type I IFN receptor-dependent pathway(s) in these regulatory events. They define a novel link between VEGF and antiviral and RLH innate immune responses and a novel pathway that regulates pulmonary VEGF activity.

Indexed as

AnimalsDEAD Box Protein 58DEAD-box RNA HelicasesDisease Models, AnimalEdemaFocal Adhesion Protein-Tyrosine KinasesImmunity, InnateInflammationInterferon Type IMiceMice, TransgenicMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CPulmonary Disease, Chronic ObstructiveDdx58 protein, mouseDEAD Box Protein 58DEAD-box RNA HelicasesFocal Adhesion Protein-Tyrosine KinasesInterferon Type IMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CToll-Like Receptor 3Vascular Endothelial Growth Factor A

Identifiers

PMID21278304
PMCPMC3114061
OpenAlexW1987657604

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.