Evidence map›Paper›PMID 24748603›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Sustained hyperoxia-induced NF-κB activation improves survival and preserves lung development in neonatal mice.

Sarah McKenna, Katherine A Michaelis, Fadeke Agboke, Thanh Liu, Kristie Han, Guang Yang, Phyllis A Dennery, Clyde J Wright

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  7. Review
  8. TGF-β and NF-κB Cross-Talk: Unexpected Encounters in the Developing Lung.American journal of respiratory cell and molecular biology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Interleukin-33 (IL-33) Increases Hyperoxia-Induced Bronchopulmonary Dysplasia in Newborn Mice by Regulation of Inflammatory Mediators.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Sex-specific differences in neonatal hyperoxic lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016
    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 3 institutions in 1 country.

Sarah McKennaSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado;
Katherine A MichaelisSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado;
Fadeke AgbokeDepartment of Pediatrics, Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
Thanh LiuSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado;
Kristie HanSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado;
Guang YangDepartment of Pediatrics, Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
Phyllis A DenneryDepartment of Pediatrics, Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Clyde J WrightSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado; clyde.wright@ucdenver.edu.
University of Colorado Denver · USChildren's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Role of Heme Oxygenase in Neonatal Hyperoxic InjuryR01HL058752 · NHLBI · STANFORD UNIVERSITY · PI DENNERY, PHYLLIS A. · 1999 to 2013
$4.5M
The unique role of IkBa in modulating NF-kB activity in the newborn lung.K08HL098562 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI WRIGHT, CLYDE JASON · 2010 to 2014
$670k
NHLBI NIH HHS HL058752-11NHLBI NIH HHS K08 HL098562
6 · The paper itself

Abstract

Oxygen toxicity contributes to the pathogenesis of bronchopulmonary dysplasia (BPD). Neonatal mice exposed to hyperoxia develop a simplified lung structure that resembles BPD. Sustained activation of the transcription factor NF-κB and increased expression of protective target genes attenuate hyperoxia-induced mortality in adults. However, the effect of enhancing hyperoxia-induced NF-κB activity on lung injury and development in neonatal animals is unknown. We performed this study to determine whether sustained NF-κB activation, mediated through IκBβ overexpression, preserves lung development in neonatal animals exposed to hyperoxia. Newborn wild-type (WT) and IκBβ-overexpressing (AKBI) mice were exposed to hyperoxia (>95%) or room air from day of life (DOL) 0-14, after which all animals were kept in room air. Survival curves were generated through DOL 14. Lung development was assessed using radial alveolar count (RAC) and mean linear intercept (MLI) at DOL 3 and 28 and pulmonary vessel density at DOL 28. Lung tissue was collected, and NF-κB activity was assessed using Western blot for IκB degradation and NF-κB nuclear translocation. WT mice demonstrated 80% mortality through 14 days of exposure. In contrast, AKBI mice demonstrated 60% survival. Decreased RAC, increased MLI, and pulmonary vessel density caused by hyperoxia in WT mice were significantly attenuated in AKBI mice. These findings were associated with early and sustained NF-κB activation and expression of cytoprotective target genes, including vascular endothelial growth factor receptor 2. We conclude that sustained hyperoxia-induced NF-κB activation improves neonatal survival and preserves lung development. Potentiating early NF-κB activity after hyperoxic exposure may represent a therapeutic intervention to prevent BPD.

Indexed as

AnimalsAnimals, NewbornGene Expression RegulationHyperoxiaI-kappa B ProteinsLungLung InjuryMiceMice, Inbred ICRNF-kappa BSignal TransductionVascular Endothelial Growth Factor Receptor-2I kappa B beta proteinI-kappa B ProteinsNF-kappa BVascular Endothelial Growth Factor Receptor-2bronchopulmonary dysplasiaIκBβ hyperoxic lung injurylung developmentNF-κB

Identifiers

PMID24748603
PMCPMC4060010
OpenAlexW2029013092

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.