Evidence map›Paper›PMID 21471107›Full record

ArticleAmerican journal of respiratory and critical care medicine2011

c-Kit is essential for alveolar maintenance and protection from emphysema-like disease in mice.

James Y Lindsey, Koustav Ganguly, David M Brass, Zhuowei Li, Erin N Potts, Simone Degan, Huaiyong Chen, Brian Brockway, Soman N Abraham, Annerose Berndt and 5 more

RetractedAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. C-KitIranian journal of basic medical sciences · 2022
    Article
  4. Tissue distribution of stem cell factor in adults.Experimental and molecular pathology · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. New Role of Adult Lung c-kitMediators of inflammation · 2016
    Article
  12. Article
  13. Secreted phosphoprotein 1 is a determinant of lung function development in mice.American journal of respiratory cell and molecular biology · 2014
    Article
  14. Article
  15. Article
  16. Review
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

James Y LindseyDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.
Koustav Ganguly
David M Brass
Zhuowei Li
Erin N Potts
Simone Degan
Huaiyong Chen
Brian Brockway
Soman N Abraham
Annerose Berndt
Barry R Stripp
W Michael Foster
George D Leikauf
Holger Schulz
John W Hollingsworth
Duke Medical Center · USUniversity of Pittsburgh · USDuke University · USHelmholtz Zentrum München · DE

Funding

Improving our mechanistic understanding of Electronic-cigarette, or vaping, product use-associated lung injuryU01ES015675 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEIKAUF, GEORGE DOUGLAS · 2006 to 2020
$8.9M
Stem Cells to Enhance Bronchiolar Reparative Capacity.R01HL090146 · NHLBI · DUKE UNIVERSITY · PI STRIPP, BARRY R · 2007 to 2010
$2.6M
OZONE PRIMES PULMONARY INNATE IMMUNITYR01ES016126 · NIEHS · OHIO STATE UNIVERSITY · PI HOLLINGSWORTH, JOHN W · 2008 to 2012
$2.3M
Growth Factor Protection in Acute Lung InjuryR01HL077763 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEIKAUF, GEORGE DOUGLAS · 2006 to 2009
$1.4M
Role of Metalloproteinases in Mucin Overproduction in COPDR01HL085655 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEIKAUF, GEORGE DOUGLAS · 2008 to 2011
$1.4M
Dependency of O-3 Induced Lung Mucus Hypersecretion on NQ01R01ES016347 · NIEHS · DUKE UNIVERSITY · PI FOSTER, W MICHAEL · 2008 to 2010
$1.0M
Functional implications of the TNFR21ES016659 · NIEHS · DUKE UNIVERSITY · PI FOSTER, W MICHAEL, HOLLINGSWORTH, JOHN W · 2008 to 2009
$419k
NHLBI NIH HHS HL077763NHLBI NIH HHS HL085655NHLBI NIH HHS HL090146NHLBI NIH HHS R01 HL085655NIEHS NIH HHS ES015675NIEHS NIH HHS ES016126NIEHS NIH HHS ES016347NIEHS NIH HHS ES016659NIEHS NIH HHS R01 ES016126NIEHS NIH HHS U01 ES015675
6 · The paper itself

Abstract

rationalePreviously, we demonstrated a candidate region for susceptibility to airspace enlargement on mouse chromosome 5. However, the specific candidate genes within this region accounting for emphysema-like changes remain unrecognized. c-Kit is a receptor tyrosine kinase within this candidate gene region that has previously been recognized to contribute to the survival, proliferation, and differentiation of hematopoietic stem cells. Increases in the percentage of cells expressing c-Kit have previously been associated with protection against injury-induced emphysema.

objectivesDetermine whether genetic variants of c-Kit are associated with spontaneous airspace enlargement.

methodsPerform single-nucleotide polymorphism association studies in the mouse strains at the extremes of airspace enlargement phenotype for variants in c-Kit tyrosine kinase. Characterize mice bearing functional variants of c-Kit compared with wild-type controls for the development of spontaneous airspace enlargement. Epithelial cell proliferation was measured in culture. MEASUREMENTS AND MAIN

resultsUpstream regulatory single-nucleotide polymorphisms in the divergent mouse strains were associated with the lung compliance difference observed between the extreme strains. c-Kit mutant mice (Kit(W-sh)/(W-sh)), when compared with genetic controls, developed altered lung histology, increased total lung capacity, increased residual volume, and increased lung compliance that persist into adulthood. c-Kit inhibition with imatinib attenuated in vitro proliferation of cells expressing epithelial cell adhesion molecule.

conclusionsOur findings indicate that c-Kit sustains and/or maintains normal alveolar architecture in the lungs of mice. In vitro data suggest that c-Kit can regulate epithelial cell clonal expansion. The precise mechanisms that c-Kit contributes to the development of airspace enlargement and increased lung compliance remain unclear and warrants further investigation.

Indexed as

AnimalsEmphysemaGenetic Predisposition to DiseaseLungLung ComplianceMiceMice, Inbred StrainsMice, Mutant StrainsPolymorphism, Single NucleotideProto-Oncogene Proteins c-kitPulmonary AlveoliProto-Oncogene Proteins c-kit

Identifiers

PMID21471107
PMCPMC3136992
OpenAlexW2101144194

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.