Evidence map›Paper›PMID 10623675›Full record

ArticleThe American journal of pathology2000

Neuroepithelial bodies of pulmonary airways serve as a reservoir of progenitor cells capable of epithelial regeneration.

S D Reynolds, A Giangreco, J H Power, B R Stripp

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

180 citing papers in PubMed, 445 citations in OpenAlex.

  1. Article
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  6. Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  13. Review
  14. Article
  15. The lung mesenchyme in development, regeneration, and fibrosis.The Journal of clinical investigation · 2023
    Review
  16. An update in club cell biology and its potential relevance to chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. Article

120 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

S D ReynoldsDepartment of Environmental Medicine, University of Rochester, Rochester, New York 14642, USA.
A Giangreco
J H Power
B R Stripp
University of Rochester · USFlinders University · AU

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
BCL-2, ROS, AND CELL DEATH IN DEVELOPMENTAL TOXICITYR01ES007026 · NIEHS · UNIVERSITY OF WASHINGTON · PI MIRKES, PHILIP E · 1996 to 2002
$1.2M
NIEHS NIH HHS ES01247NIEHS NIH HHS ES07026NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES007026NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

Remodeling of the conducting airway epithelium is a common finding in the chronically injured lung and has been associated with increased risk for developing lung cancer. Pulmonary neuroendocrine cells and clusters of these cells termed neuroepithelial bodies (NEBs) play a central role in each of these processes. We previously developed an adult mouse model of airway injury and repair in which epithelial regeneration after naphthalene-induced Clara cell ablation occurred preferentially at airway branch points and gave rise to nascent Clara cells. Continued repair was accompanied by NEB hyperplasia. We now provide the following evidence that the NEB microenvironment serves as a source of airway progenitor cells that contribute to focal regeneration of the airway epithelium: 1) nascent Clara cells and NEBs localize to the same spatial domain; 2) within NEB, both Clara cell secretory protein- and calcitonin gene-related peptide-immunopositive cells are proliferative; 3) the NEB microenvironment of both the steady-state and repairing lung includes cells that are dually immunopositive for Clara cell secretory protein and calcitonin gene-related peptide, which were previously identified only within the embryonic lung; and 4) NEBs harbor variant Clara cells deficient in cytochrome P450 2F2-immunoreactive protein. These data suggest that the NEB microenvironment is a reservoir of pollutant-resistant progenitor cells responsive to depletion of an abundant airway progenitor such as the Clara cell.

Indexed as

UteroglobinAnimalsCalcitonin Gene-Related PeptideCell AggregationEpitheliumImmunohistochemistryLungMaleMiceMitosisNeurosecretory SystemsProteinsReference ValuesRegenerationStem CellsCalcitonin Gene-Related PeptideProteinsScgb1a1 protein, mouseUteroglobin

Identifiers

PMID10623675
PMCPMC1868636
OpenAlexW2119835285

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.