Evidence map›Paper›PMID 19520907›Full record

ArticleAmerican journal of respiratory and critical care medicine2009

Pulmonary epithelial neuropilin-1 deletion enhances development of cigarette smoke-induced emphysema.

Anne Le, Rachel Zielinski, Chaoxia He, Michael T Crow, Shyam Biswal, Rubin M Tuder, Patrice M Becker

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. VEGF (Vascular Endothelial Growth Factor) and Fibrotic Lung Disease.International journal of molecular sciences · 2018
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Expression of semaphorin 3A and neuropilin 1 in asthma.Journal of Korean medical science · 2013
    Article
  14. Article
  15. Article
  16. Neuropilins: expression and roles in the epithelium.International journal of experimental pathology · 2012
    Review
  17. Article
  18. Involvement of ceramide in cell death responses in the pulmonary circulation.Proceedings of the American Thoracic Society · 2011
    Review
  19. Stress responses affecting homeostasis of the alveolar capillary unit.Proceedings of the American Thoracic Society · 2011
    Review
  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 2 institutions in 1 country.

Anne LeDivision of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Rachel Zielinski
Chaoxia He
Michael T Crow
Shyam Biswal
Rubin M Tuder
Patrice M Becker
Pulmonary and Critical Care Associates · USJohns Hopkins University · US

Funding

Sleep Related Mechanisms of COPD ProgressionP50HL084945 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WISE, ROBERT A. · 2007 to 2011
$15.1M
Endothelial Cell Death in EmphysemaR01HL066554 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M · 2000 to 2007
$2.6M
Modifier Role of Nrf2 in Lung Injury and EmphysemaR01HL081205 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BISWAL, SHYAM · 2005 to 2009
$2.0M
Neuropilin-1 and VEGF-mediated pulmonary edemaR01HL083286 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, PATRICE M · 2006 to 2009
$1.6M
NHLBI NIH HHS P50HL084945NHLBI NIH HHS R01HL066554NHLBI NIH HHS R01HL081205NHLBI NIH HHS R01HL083286
6 · The paper itself

Abstract

rationaleCigarette smoke (CS) exposure is an important risk factor for chronic obstructive pulmonary disease; however, not all smokers develop disease, suggesting that other factors influence disease development.

objectivesWe sought to determine whether neuropilin-1 (Nrp1), an integral component of receptor complexes mediating alveolar septation and vascular development, was involved in maintenance of normal alveolar structure, and/or altered susceptibility to the effects of CS.

methodsTransgenic mice were generated to achieve inducible lung-specific deletion of epithelial Nrp1. We determined whether conditional Nrp1 deletion altered airspace size, then compared the effects of chronic CS or filtered air exposure on airspace size, inflammation, and the balance between cell death and proliferation in conditionally Nrp1-deficient adult mice and littermate controls. Finally, we evaluated the effects of Nrp1 silencing on cell death after acute exposure of A549 cells to cigarette smoke extract or short chain ceramides. MEASUREMENTS AND MAIN

resultsGenetic deletion of epithelial Nrp1 in either postnatal or adult lungs resulted in a small increase in airspace size. More notably, both airspace enlargement and apoptosis of type I and type II alveolar epithelial cells were significantly enhanced following chronic CS exposure in conditionally Nrp1-deficient adult mice. Silencing of Nrp1 in A549 cells did not alter cell survival after vehicle treatment but significantly augmented apoptosis after exposure to cigarette smoke extract or ceramide.

conclusionsThese data support a role for epithelial Nrp1 in the maintenance of normal alveolar structure and suggest that dysregulation of Nrp1 expression may promote epithelial cell death in response to CS exposure, thereby enhancing emphysema development.

Indexed as

Gene DeletionAnimalsApoptosisCell ProliferationDisease Models, AnimalEmphysemaMiceMice, TransgenicNeuropilin-1Pulmonary AlveoliRandom AllocationReference ValuesRespiratory MucosaSmokingVascular Endothelial Growth Factor ANeuropilin-1Vascular Endothelial Growth Factor A

Identifiers

PMID19520907
PMCPMC2742758
OpenAlexW2167045140

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.