Evidence map›Paper›PMID 21216975›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

A role for matrix metalloproteinase 9 in IFNγ-mediated injury in developing lungs: relevance to bronchopulmonary dysplasia.

Anantha Harijith, Rayman Choo-Wing, Sule Cataltepe, Ryuji Yasumatsu, Zubair H Aghai, Joakim Janér, Sture Andersson, Robert J Homer, Vineet Bhandari

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Genetic Deletion ofInternational journal of molecular sciences · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. [Methods for establishing animal model of bronchopulmonary dysplasia and their evaluation].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017
    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

9 authors at 4 institutions in 3 countries.

Anantha HarijithDivision of Perinatal Medicine, Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06520-8064, USA.
Rayman Choo-Wing
Sule Cataltepe
Ryuji Yasumatsu
Zubair H Aghai
Joakim Janér
Sture Andersson
Robert J Homer
Vineet Bhandari
Yale University · USBrigham and Women's Hospital · USUniversity of Helsinki · FIRutgers, The State University of New Jersey · US

Funding

Role of Angiogenic Agents in Alveolar Maturation and InjuryR01HL085103 · NHLBI · YALE UNIVERSITY · PI BHANDARI, VINEET · 2009 to 2013
$2.0M
Analysis of Airway Serpins in Baboon Models of BPDU01HL075904 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI CATALTEPE, SULE · 2003 to 2005
$748k
Angiogenic Agents and Alveolar InjuryK08HL074195 · NHLBI · YALE UNIVERSITY · PI BHANDARI, VINEET · 2003 to 2007
$664k
NHLBI NIH HHS HL075904NHLBI NIH HHS HL-74195NHLBI NIH HHS HL-85103
6 · The paper itself

Abstract

We noted a marked increase in IFNγ mRNA in newborn (NB) murine lungs after exposure to hyperoxia. We sought to evaluate the role of IFNγ in lung injury in newborns. Using a unique triple-transgenic (TTG), IFNγ-overexpressing, lung-targeted, externally regulatable NB murine model, we describe a lung phenotype of impaired alveolarization, resembling human bronchopulmonary dysplasia (BPD). IFNγ-mediated abnormal lung architecture was associated with increased cell death and the upregulation of cell death pathway mediators caspases 3, 6, 8, and 9, and angiopoietin 2. Moreover, an increase was evident in cathepsins B, H, K, L, and S, and in matrix metalloproteinases (MMPs) 2, 9, 12, and 14. The IFNγ-mediated abnormal lung architecture was found to be MMP9-dependent, as indicated by the rescue of the IFNγ-induced pulmonary phenotype and survival during hyperoxia with a concomitant partial deficiency of MMP9. This result was concomitant with a decrease in caspases 3, 6, 8, and 9 and angiopoietin 2, but an increase in the expression of angiopoietin 1. In addition, NB IFNγ TTG mice exhibited significantly decreased survival during hyperoxia, compared with littermate controls. Furthermore, as evidence of clinical relevance, we show increased concentrations of the downstream targets of IFNγ chemokine (C-X-C motif) ligands (CXCL10 and CXCL11) in baboon and human lungs with BPD. IFNγ and its downstream targets may contribute significantly to the final common pathway of hyperoxia-induced injury in the developing lung and in human BPD.

Indexed as

Gene Expression Regulation, EnzymologicAngiopoietinsAnimalsBronchopulmonary DysplasiaCaspasesCathepsinsChemokinesDisease Models, AnimalHumansHyperoxiaInfant, NewbornInterferon-gammaLung InjuryMatrix Metalloproteinase 9MiceMice, Inbred C57BLAngiopoietinsCaspasesCathepsinsChemokinesInterferon-gammaMatrix Metalloproteinase 9

Identifiers

PMID21216975
PMCPMC3095982
OpenAlexW2062192476

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.