Evidence map›Paper›PMID 22096573›Full record

ArticlePloS one2011

Semaphorin 3A contributes to distal pulmonary epithelial cell differentiation and lung morphogenesis.

Patrice M Becker, Tracy S Tran, Michael J Delannoy, Chaoxia He, John M Shannon, Sharon McGrath-Morrow

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  9. Successful Establishment of Primary Type II Alveolar Epithelium with 3D Organotypic Coculture.American journal of respiratory cell and molecular biology · 2018
    Article
  10. Article
  11. Review
  12. Article
  13. Chronic allograft rejection: a fresh look.Current opinion in organ transplantation · 2015
    Review
  14. Review
  15. Expression of semaphorin 3A and neuropilin 1 in asthma.Journal of Korean medical science · 2013
    Article
  16. Functional genomic assessment of phosgene-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2013
    Article
  17. Article
  18. 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

6 authors at 3 institutions in 1 country.

Patrice M BeckerDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America. Patrice.Becker@questcor.com
Tracy S Tran
Michael J Delannoy
Chaoxia He
John M Shannon
Sharon McGrath-Morrow
Johns Hopkins University · USJohns Hopkins Medicine · USCincinnati Children's Hospital Medical Center · US

Funding

LPCAT1 is essential for perinatal lung function and survivalR01HL098319 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI SHANNON, JOHN M · 2010 to 2013
$1.9M
Neuropilin-1 and VEGF-mediated pulmonary edemaR01HL083286 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, PATRICE M · 2006 to 2009
$1.6M
NHLBI NIH HHS R01 HL083286NHLBI NIH HHS R01HL083286NHLBI NIH HHS R01 HL098319NHLBI NIH HHS R01HL098319
6 · The paper itself

Abstract

rationaleSemaphorin 3A (Sema3A) is a neural guidance cue that also mediates cell migration, proliferation and apoptosis, and inhibits branching morphogenesis. Because we have shown that genetic deletion of neuropilin-1, which encodes an obligatory Sema3A co-receptor, influences airspace remodeling in the smoke-exposed adult lung, we sought to determine whether genetic deletion of Sema3A altered distal lung structure.

methodsTo determine whether loss of Sema3A signaling influenced distal lung morphology, we compared pulmonary histology, distal epithelial cell morphology and maturation, and the balance between lung cell proliferation and death, in lungs from mice with a targeted genetic deletion of Sema3A (Sema3A(-/-)) and wild-type (Sema3A(+/+)) littermate controls.

resultsGenetic deletion of Sema3A resulted in significant perinatal lethality. At E17.5, lungs from Sema3A(-/-) mice had thickened septae and reduced airspace size. Distal lung epithelial cells had increased intracellular glycogen pools and small multivesicular and lamellar bodies with atypical ultrastructure, as well as reduced expression of type I alveolar epithelial cell markers. Alveolarization was markedly attenuated in lungs from the rare Sema3A(-/-) mice that survived the immediate perinatal period. Furthermore, Sema3A deletion was linked with enhanced postnatal alveolar septal cell death.

conclusionsThese data suggest that Sema3A modulates distal pulmonary epithelial cell development and alveolar septation. Defining how Sema3A influences structural plasticity of the developing lung is a critical first step for determining if this pathway can be exploited to develop innovative strategies for repair after acute or chronic lung injury.

Indexed as

AnimalsCell DifferentiationEpithelial CellsImmunohistochemistryLungMiceMice, Inbred C57BLMice, Mutant StrainsMorphogenesisOrganogenesisSemaphorin-3ASemaphorin-3A

Identifiers

PMID22096573
PMCPMC3214054
OpenAlexW1982825249

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LicenceCC BY
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Registered trials

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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.