Evidence map›Paper›PMID 18441284›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

Developmental regulation of NO-mediated VEGF-induced effects in the lung.

Vineet Bhandari, Rayman Choo-Wing, Chun G Lee, Kamran Yusuf, Jonathan H Nedrelow, Namasivayam Ambalavanan, Herbert Malkus, Robert J Homer, Jack A Elias

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  15. Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia.Birth defects research. Part A, Clinical and molecular teratology · 2014
    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

9 authors at 4 institutions in 2 countries.

Vineet BhandariDivision of Perinatal Medicine, Yale University School of Medicine, Department of Pediatrics, New Haven, CT 06520-8057, USA. vineet.bhandari@yale.edu
Rayman Choo-Wing
Chun G Lee
Kamran Yusuf
Jonathan H Nedrelow
Namasivayam Ambalavanan
Herbert Malkus
Robert J Homer
Jack A Elias
Perinatal Institute · GBPulmonary and Critical Care Associates · USYale University · USUniversity of Alabama · US

Funding

Unique role of lung dendritic cells in Th2 responsesP01HL056389 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2002 to 2006
$10.2M
TRANSGENIC MODELING OF AIRWAY INFLAMMATION IN ASTHMAP50HL056389 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 1997 to 2001
$4.0M
TRANSGENIC MODELING OF TH1/TH2 RESPONSES IN ASTHMAR01HL061904 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 1998 to 2001
$736k
Angiogenic Agents and Alveolar InjuryK08HL074195 · NHLBI · YALE UNIVERSITY · PI BHANDARI, VINEET · 2003 to 2007
$664k
NHLBI NIH HHS HL-56389NHLBI NIH HHS HL-61904NHLBI NIH HHS HL-64642NHLBI NIH HHS HL-74195NICHD NIH HHS HD-07049
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is known to have a pivotal role in lung development and in a variety of pathologic conditions in the adult lung. Our earlier studies have shown that NO is a critical mediator of VEGF-induced vascular and extravascular effects in the adult murine lung. As significant differences have been reported in the cytokine responses in the adult versus the neonatal lung, we hypothesized that there may be significant differences in VEGF-induced alterations in the developing as opposed to the mature lung. Furthermore, nitric oxide (NO) mediation of these VEGF-induced effects may be developmentally regulated. Using a novel externally regulatable lung-targeted transgenic murine model, we found that VEGF-induced pulmonary hemorrhage was mediated by NO-dependent mechanisms in adults and newborns. VEGF enhanced surfactant production in adults as well as increased surfactant and lung development in newborns, via an NO-independent mechanism. While the enhanced survival in hyperoxia in the adult was partly NO-dependent, there was enhanced hyperoxia-induced lung injury in the newborn. In addition, human amniotic fluid VEGF levels correlated positively with surfactant phospholipids. Tracheal aspirate VEGF levels had an initial spike, followed by a decline, and then a subsequent rise, in human neonates with an outcome of bronchopulmonary dysplasia or death. Our data show that VEGF can have injurious as well as potentially beneficial developmental effects, of which some are NO dependent, others NO independent. This opens up the possibility of selective manipulation of any VEGF-based intervention using NO inhibitors for maximal potential clinical benefit.

Indexed as

Amniotic FluidAnimalsAnimals, NewbornBronchopulmonary DysplasiaCapillary PermeabilityFemaleHemorrhageHumansHyperoxiaInfant, NewbornLungLung DiseasesMiceMice, TransgenicNitric OxidePregnancyNitric OxidePulmonary SurfactantsVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID18441284
PMCPMC2551703
OpenAlexW2103911567

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.