Evidence map›Paper›PMID 27036872›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Hepatocyte growth factor as a downstream mediator of vascular endothelial growth factor-dependent preservation of growth in the developing lung.

Gregory Seedorf, Alexander J Metoxen, Robert Rock, Neil Markham, Sharon Ryan, Thiennu Vu, Steven H Abman

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. 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
4.9field-weighted citation impact, top 5% 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, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Stem cell-based therapy for human diseases.Signal transduction and targeted therapy · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Chronic lung diseases: prospects for regeneration and repair.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  11. Review
  12. Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  13. Article
  14. Article
  15. Observational
  16. Article
  17. Review
  18. NMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  19. Article
  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

7 authors at 3 institutions in 1 country.

Gregory SeedorfPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and gregory.seedorf@ucdenver.edu.
Alexander J MetoxenPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and.
Robert RockPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and.
Neil MarkhamPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and.
Sharon RyanPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and.
Thiennu VuDepartment of Medicine, University of California, San Francisco, California.
Steven H AbmanPediatric Heart Lung Center and Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado; and.
University of Colorado Denver · USUniversity of Colorado Anschutz Medical Campus · USUniversity of California, San Francisco · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Role of VEGF in Perinatal Pulmonary HypertensionR01HL068702 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT, SHEPHERD, DOUGLAS · 2001 to 2021
$6.7M
ACADEMIC TRAINING PROGRAM IN PEDIATRIC PULMONARY DISEASET32HL007670 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT · 1988 to 2019
$5.9M
Pediatric Pulmonology and Hematology Research Training for Medical StudentsT35HL112930 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT, DI PAOLA, JORGE A · 2012 to 2015
$67k
NCI NIH HHS P30 CA046934NHLBI NIH HHS R01 HL068702NHLBI NIH HHS T32 HL007670NHLBI NIH HHS T35 HL112930
6 · The paper itself

Abstract

Impaired vascular endothelial growth factor (VEGF) signaling contributes to the pathogenesis of bronchopulmonary dysplasia (BPD). We hypothesized that the effects of VEGF on lung structure during development may be mediated through its downstream effects on both endothelial nitric oxide synthase (eNOS) and hepatocyte growth factor (HGF) activity, and that, in the absence of eNOS, trophic effects of VEGF would be mediated through HGF signaling. To test this hypothesis, we performed an integrative series of in vitro (fetal rat lung explants and isolated fetal alveolar and endothelial cells) and in vivo studies with normal rat pups and eNOS(-/-) mice. Compared with controls, fetal lung explants from eNOS(-/-) mice had decreased terminal lung bud formation, which was restored with recombinant human VEGF (rhVEGF) treatment. Neonatal eNOS(-/-) mice were more susceptible to hyperoxia-induced inhibition of lung growth than controls, which was prevented with rhVEGF treatment. Fetal alveolar type II (AT2) cell proliferation was increased with rhVEGF treatment only with mesenchymal cell (MC) coculture, and these effects were attenuated with anti-HGF antibody treatment. Unlike VEGF, HGF directly stimulated isolated AT2 cells even without MC coculture. HGF directly stimulates fetal pulmonary artery endothelial cell growth and tube formation, which is attenuated by treatment with JNJ-38877605, a c-Met inhibitor. rHGF treatment preserves alveolar and vascular growth after postnatal exposure to SU-5416, a VEGF receptor inhibitor. We conclude that the effects of VEGF on AT2 and endothelial cells during lung development are partly mediated through HGF-c-Met signaling and speculate that reciprocal VEGF-HGF signaling between epithelia and endothelia is disrupted in infants who develop BPD.

Indexed as

Alveolar Epithelial CellsAnimalsCell AdhesionCells, CulturedCoculture TechniquesEndothelial CellsEndothelium, VascularFemaleHepatocyte Growth FactorLungMaleMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIIPulmonary ArterySheepHepatocyte Growth FactorHGF protein, mouseNitric Oxide Synthase Type IIINos3 protein, mouseVascular Endothelial Growth Factor Abronchopulmonary dysplasiaendothelial nitric oxide synthasehepatocyte growth factorlung developmentlung hypoplasianitric oxidevascular endothelial growth factor

Identifiers

PMID27036872
PMCPMC4935471
OpenAlexW2328191259

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.