Evidence map›Paper›PMID 23624331›Full record

ArticleFree radical biology & medicine2013

Cyclooxygenase-2 in newborn hyperoxic lung injury.

Rodney D Britt, Markus Velten, Trent E Tipple, Leif D Nelin, Lynette K Rogers

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2013. 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
2.4field-weighted citation impact, top 11% 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, 30 citations in OpenAlex.

  1. Article
  2. Article
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  5. Cyclooxygenase-2 deficiency attenuates lipopolysaccharide-induced inflammation, apoptosis, and acute lung injury in adult mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
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  7. Review
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  15. Iloprost attenuates hyperoxia-mediated impairment of lung development in newborn mice.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  16. [Association between high-mobility group box 1 and neonatal respiratory distress syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017
    Article
  17. Review
  18. Article
  19. CD11b(+) Mononuclear Cells Mitigate Hyperoxia-Induced Lung Injury in Neonatal Mice.American journal of respiratory cell and molecular biology · 2016
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  20. 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 1 country.

Rodney D BrittCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43205, USA.
Markus VeltenDepartment of Anesthesiology and Intensive Care Medicine, Rheinische Friedrich-Wilhlems-University, University Medical Center, Bonn, Germany.
Trent E TippleCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43205, USA; Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH 43215, USA.
Leif D NelinCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43205, USA; Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH 43215, USA.
Lynette K RogersCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43205, USA; Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH 43215, USA. Electronic address: Lynette.Rogers@NationwideChildrens.org.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

DHA attenuates Inflammatory Responses Through Altering RAGE SignalingR01AT006880 · NCCIH · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROGERS, LYNETTE KAY · 2011 to 2015
$1.8M
Regulation of Lung Growth and Development by Thioredoxin Interacting ProteinK08HL093365 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI TIPPLE, TRENT · 2010 to 2012
$399k
Lipoxin-Mediated Inflammatory Resolution in Newborn Hyperoxic Lung InjuryF31HL097619 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI BRITT, RODNEY · 2009 to 2012
$99k
NCCIH NIH HHS R01 AT006880NCCIH NIH HHS R01AT006880NHLBI NIH HHS F31 HL097619NHLBI NIH HHS F31HL097619NHLBI NIH HHS K08 HL093365NHLBI NIH HHS K08HL093365-03
6 · The paper itself

Abstract

Supraphysiological O2 concentrations, mechanical ventilation, and inflammation significantly contribute to the development of bronchopulmonary dysplasia (BPD).Exposure of newborn mice to hyperoxia causes inflammation and impaired alveolarization similar to that seen in infants with BPD.Previously, we demonstrated that pulmonary cyclooxygenase-2 (COX-2) protein expression is increased in hyperoxia-exposed newborn mice.The present studies were designed to define the role of COX-2 in newborn hyperoxic lung injury.We tested the hypothesis that attenuation of COX-2 activity would reduce hyperoxia-induced inflammation and improve alveolarization.Newborn C3H/HeN micewere injected daily with vehicle, aspirin (nonselective COX-2 inhibitor), or celecoxib (selective COX-2 inhibitor) for the first 7 days of life.Additional studies utilized wild-type (C57Bl/6, COX-2(+/+)), heterozygous (COX-2(+/-)), and homozygous (COX-2(-/-)) transgenic mice.Micewere exposed to room air (21% O2) or hyperoxia (85% O2) for 14 days.Aspirin-injected and COX-2(-/-) pups had reduced levels of monocyte chemoattractant protein (MCP-1) in bronchoalveolar lavage fluid (BAL).Both aspirin and celecoxib treatment reduced macrophage numbers in the alveolar walls and air spaces.Aspirin and celecoxib treatment attenuated hyperoxia-induced COX activity, including altered levels of prostaglandin (PG)D2 metabolites.Decreased COX activity, however, did not prevent hyperoxia-induced lung developmental deficits.Our data suggest thatincreased COX-2 activity may contribute to proinflammatory responses, including macrophage chemotaxis, during exposure to hyperoxia.Modulation of COX-2 activity may be a useful therapeutic target to limit hyperoxia-induced inflammation in preterm infants at risk of developing BPD.

Indexed as

AnimalsAnimals, NewbornBody WeightCyclooxygenase 2HyperoxiaIntramolecular OxidoreductasesLipocalinsLung InjuryMiceMice, Inbred C3HProstaglandin-E SynthasesCyclooxygenase 2Intramolecular OxidoreductasesLipocalinsProstaglandin-E Synthasesprostaglandin R2 D-isomerasePtgs2 protein, mouseBronchopulmonary dysplasiaCyclooxygenase-2HyperoxiaProstaglandins

Identifiers

PMID23624331
PMCPMC3752000
OpenAlexW2068260789

What OpenQuestion holds

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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.