Evidence map›Paper›PMID 24673633›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Superoxide dismutase 3 dysregulation in a murine model of neonatal lung injury.

Hataya K Poonyagariyagorn, Shana Metzger, Dustin Dikeman, Armando Lopez Mercado, Alla Malinina, Carla Calvi, Sharon McGrath-Morrow, Enid R Neptune

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Lung SOD3 limits neurovascular reperfusion injury and systemic immune activation following transient global cerebral ischemia.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2020
    Article
  10. Article
  11. Bronchopulmonary dysplasia: Pathogenesis and treatment.Experimental and therapeutic medicine · 2018
    Review
  12. Extracellular matrix in lung development, homeostasis and disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Hataya K Poonyagariyagorn1 Division of Pulmonary and Critical Care Medicine and.
Shana Metzger
Dustin Dikeman
Armando Lopez Mercado
Alla Malinina
Carla Calvi
Sharon McGrath-Morrow
Enid R Neptune
Johns Hopkins University · USPulmonary and Critical Care Associates · US

Funding

Regulation of Cardiac Calcium Channels by an Autoinhibitory Signalling ComplexR01HL085372 · NHLBI · UNIVERSITY OF WASHINGTON · PI CATTERALL, WILLIAM A · 2007 to 2016
$3.5M
Resolution of Diffuse Inflammatory Lung Injury in Neonatal MiceR01HL114800 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MCGRATH-MORROW, SHARON ANN · 2013 to 2021
$3.3M
NHLBI NIH HHS R01 HL085372NHLBI NIH HHS R01HL085372NHLBI NIH HHS R01 HL114800
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD), a common chronic respiratory disease that occurs after premature birth, is believed to be secondary to oxidative damage from hyperoxia and inflammation, which leads to impaired alveolar formation and chronic lung dysfunction. We hypothesized that extracellular superoxide dismutase (SOD)3, an antioxidant uniquely targeted to the extracellular matrix (ECM) and alveolar fluid, might have a different response (down-regulation) to hyperoxic injury and recovery in room air (RA), thereby contributing to the persistent airspace injury and inflammation. We used a murine BPD model using postnatal hyperoxia (O2) (4 or 5 d) followed by short-term recovery (14 d) in RA, which mimics the durable effects after injury during alveolar development. This was associated with significantly increased mRNA expression for antioxidant genes mediated by nuclear factor erythroid 2-related factor (Nrf2) in the O2 (n = 4) versus RA group (n = 5). SOD3, an Nrf2-independent antioxidant, was significantly reduced in the O2-exposed mice compared with RA. Immunohistochemistry revealed decreased and disrupted SOD3 deposition in the alveolar ECM of O2-exposed mice. Furthermore, this distinct hyperoxic antioxidant and injury profile was reproducible in murine lung epithelial 12 cells exposed to O2. Overexpression of SOD3 rescued the injury measures in the O2-exposed cells. We establish that reduced SOD3 expression correlates with alveolar injury measures in the recovered neonatal hyperoxic lung, and SOD3 overexpression attenuates hyperoxic injury in an alveolar epithelial cell line. Such findings suggest a candidate mechanism for the pathogenesis of BPD that may lead to targeted interventions.

Indexed as

Gene Expression ProfilingGene Expression Regulation, EnzymologicAnimalsAnimals, NewbornAntioxidantsBronchopulmonary DysplasiaFemaleHyperoxiaInflammationLungLung InjuryMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2OxygenAntioxidantsNfe2l2 protein, mouseNF-E2-Related Factor 2OxygenSod3 protein, mouseSuperoxide Dismutasebronchopulmonary dysplasiaextracellular superoxide dismutasehyperoxia, murine lung epithelial 12Nrf-2

Identifiers

PMID24673633
PMCPMC4189488
OpenAlexW2050251117

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.