Evidence map›Paper›PMID 24571919›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Genome-wide association mapping of acute lung injury in neonatal inbred mice.

Jennifer L Nichols, Wesley Gladwell, Kirsten C Verhein, Hye-Youn Cho, Jürgen Wess, Oscar Suzuki, Tim Wiltshire, Steven R Kleeberger

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Genetic determinants of ammonia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  4. Article
  5. Aurothioglucose enhances proangiogenic pathway activation in lungs from room air and hyperoxia-exposed newborn mice.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Genetic determinants of susceptibility to silver nanoparticle-induced acute lung inflammation in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  10. Article
  11. Article
  12. Macrophage epoxygenase determines a profibrotic transcriptome signature.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  13. Article
  14. Article
  15. 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

8 authors at 4 institutions in 1 country.

Jennifer L NicholsLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, U.S. National Institutes of Health, Research Triangle Park, North Carolina, USA; Curriculum in Toxicology, Center for Environmental Medicine, Asthma, and Lung Biology, and.
Wesley GladwellLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, U.S. National Institutes of Health, Research Triangle Park, North Carolina, USA;
Kirsten C VerheinLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, U.S. National Institutes of Health, Research Triangle Park, North Carolina, USA;
Hye-Youn ChoLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, U.S. National Institutes of Health, Research Triangle Park, North Carolina, USA;
Jürgen WessLaboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, U.S. National Institutes of Health, Bethesda, Maryland, USA.
Oscar SuzukiDivision of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina, USA; and.
Tim WiltshireDivision of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina, USA; and.
Steven R KleebergerLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, U.S. National Institutes of Health, Research Triangle Park, North Carolina, USA; kleeber1@niehs.nih.gov.
National Institute of Environmental Health Sciences · USNational Institutes of Health · USUniversity of North Carolina at Chapel Hill · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
The Role Of Nrf2 In Susceptibility To Hyperoxic Lung InjuryZIAES100513 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2009 to 2021
$11.5M
Muscarinic acetylcholine receptor subtypes: physiological rolesZIADK075020 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WESS, JURGEN · 2009 to 2025
$6.1M
Intramural NIH HHSNIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Reactive oxygen species (ROS) contribute to the pathogenesis of many acute and chronic pulmonary disorders, including bronchopulmonary dysplasia (BPD), a respiratory condition that affects preterm infants. However, the mechanisms of susceptibility to oxidant stress in neonatal lungs are not completely understood. We evaluated the role of genetic background in response to oxidant stress in the neonatal lung by exposing mice from 36 inbred strains to hyperoxia (95% O2) for 72 h after birth. Hyperoxia-induced lung injury was evaluated by using bronchoalveolar lavage fluid (BALF) analysis and pathology. Statistically significant interstrain variation was found for BALF inflammatory cells and protein (heritability estimates range: 33.6-55.7%). Genome-wide association mapping using injury phenotypes identified quantitative trait loci (QTLs) on chromosomes 1, 2, 4, 6, and 7. Comparative mapping of the chromosome 6 QTLs identified Chrm2 (cholinergic receptor, muscarinic 2, cardiac) as a candidate susceptibility gene, and mouse strains with a nonsynonymous coding single-nucleotide polymorphism (SNP) in Chrm2 that causes an amino acid substitution (P265L) had significantly reduced hyperoxia-induced inflammation compared to strains without the SNP. Further, hyperoxia-induced lung injury was significantly reduced in neonatal mice with targeted deletion of Chrm2, relative to wild-type controls. This study has important implications for understanding the mechanisms of oxidative lung injury in neonates.

Indexed as

AnimalsAnimals, NewbornBronchopulmonary DysplasiaFemaleGene DeletionGenome-Wide Association StudyHyperoxiaLung InjuryMaleMiceMice, Inbred StrainsPneumoniaPolymorphism, Single NucleotideQuantitative Trait LociReceptor, Muscarinic M2Receptor, Muscarinic M2bronchopulmonary dysplasiacardiaccholinergic receptorinflammationmuscarinic 2quantitative trait locus

Identifiers

PMID24571919
PMCPMC4021442
OpenAlexW2168523319

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.