Evidence map›Paper›PMID 18385079›Full record

ArticleInvestigative ophthalmology & visual science2008

Activated NAD(P)H oxidase from supplemental oxygen induces neovascularization independent of VEGF in retinopathy of prematurity model.

Yuta Saito, Abhineet Uppal, Grace Byfield, Steven Budd, M Elizabeth Hartnett

Open access · greenAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
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  4. Pathophysiology of Retinopathy of Prematurity.Annual review of vision science · 2023
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  20. 17β-estradiol ameliorates oxygen-induced retinopathy in the early hyperoxic phase.Biochemical and biophysical research communications · 2015
    Article
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

5 authors at 2 institutions in 2 countries.

Yuta SaitoDepartment of Ophthalmology, Showa University, Tokyo, Japan.
Abhineet Uppal
Grace Byfield
Steven Budd
M Elizabeth Hartnett
University of North Carolina at Chapel Hill · USShowa University · JP

Funding

Mechanisms of Angiogenesis of Retinopathy of PrematurityR01EY015130 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Mary Elizabeth Ruth Hartnett · 2005 to 2026
$7.6M
NEI NIH HHS R01 EY015130
6 · The paper itself

Abstract

purposeTo study NAD(P)H oxidase-dependent outcomes after oxygen stresses that are similar to those experienced by preterm infants today using a rat model of retinopathy of prematurity.

methodsWithin 4 hours of birth, pups and their mothers were cycled between 50% and 10% oxygen daily for 14 days and were returned to room air (21% O2, 50/10 oxygen-induced retinopathy [OIR]) or supplemental oxygen (28% O2, 50/10 OIR+SO) for 4 days. Pups received intraperitoneal injections of the specific NAD(P)H oxidase inhibitor apocynin (10 mg/kg/d) or of PBS from postnatal day (P)12 to P17, and some received intraperitoneal injections of hypoxyprobe before kill. Intravitreous neovascularization (IVNV), avascular/total retinal areas, vascular endothelial growth factor (VEGF), NAD(P)H oxidase activity, or hypoxic retina (conjugated hypoxyprobe) were determined in neurosensory retinas. Human retinal microvascular endothelial cells (RMVECs) treated with apocynin or control were exposed to 1% or 21% O2 and assayed for phosphorylated (p-)Janus kinase (JNK) and NAD(P)H oxidase activity.

resultsRetinas from 50/10 OIR+SO had increased NAD(P)H oxidase activity and lower VEGF than did retinas from 50/10 OIR. Apocynin treatment reduced the IVNV area and hypoxic retina in 50/10 OIR+SO. RMVECs treated with 1% O2 had increased p-JNK compared with RMVECs exposed to room air.

conclusionsDifferent oxygen stresses activate NAD(P)H oxidase to varying degrees to trigger disparate pathways (angiogenesis or apoptosis). The oxygen stresses and outcomes used in this study are relevant to human ROP and may explain some of the complexity in the pathophysiology of ROP resulting from oxygen exposure.

Indexed as

Disease Models, AnimalAnimalsAnimals, NewbornBlotting, WesternEndothelium, VascularEnzyme ActivationEnzyme InhibitorsEnzyme-Linked Immunosorbent AssayExtracellular Signal-Regulated MAP KinasesHumansHyperoxiaImmunoprecipitationInfant, NewbornInjections, IntraperitonealJanus KinasesNADPH OxidasesEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesJanus KinasesNADPH OxidasesOxygenProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID18385079
PMCPMC2362384
OpenAlexW1966632353

What OpenQuestion holds

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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.