Evidence map›Paper›PMID 23609017›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2013

Bone marrow cells expressing clara cell secretory protein increase epithelial repair after ablation of pulmonary clara cells.

Martha L Bustos, Marco Mura, Paula Marcus, David Hwang, Olga Ludkovski, Amy P Wong, Thomas K Waddell

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. SCGB1A1 as a Key Regulator of Splenic Immune Dysfunction in COPD: Insights From a Murine Model.International journal of chronic obstructive pulmonary disease · 2025
    Article
  2. Article
  3. Review
  4. Cell-Based Therapeutic Approaches for Cystic Fibrosis.International journal of molecular sciences · 2020
    Review
  5. Partial Restoration of CFTR Function in cftr-Null Mice following Targeted Cell Replacement Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Depletion of bone marrow CCSP-expressing cells delays airway regeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    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.

Martha L BustosDivision of Thoracic Surgery, Latner Thoracic Surgery Research Laboratories and McEwen Centre for Regenerative Medicine, University of Toronto, Toronto General Hospital, Toronto Medical Discovery Tower, Toronto, Ontario, Canada.
Marco Mura
Paula Marcus
David Hwang
Olga Ludkovski
Amy P Wong
Thomas K Waddell
University of Toronto · CAToronto General Hospital · CAPrincess Margaret Cancer Centre · CA

Funding

Canadian Institutes of Health Research MOP 86760
6 · The paper itself

Abstract

We have previously reported a subpopulation of bone marrow cells (BMC) that express Clara cell secretory protein (CCSP), generally felt to be specific to lung Clara cells. Ablation of lung Clara cells has been reported using a transgenic mouse that expresses thymidine kinase under control of the CCSP promoter. Treatment with ganciclovir results in permanent elimination of CCSP(+) cells, failure of airway regeneration, and death. To determine if transtracheal delivery of wild-type bone marrow CCSP(+) cells is beneficial after ablation of lung CCSP(+) cells, transgenic mice were treated with ganciclovir followed by transtracheal administration of CCSP(+) or CCSP(-) BMC. Compared with mice administered CCSP(-) cells, mice treated with CCSP(+) cells had more donor cells lining the airway epithelium, where they expressed epithelial markers including CCSP. Although donor CCSP(+) cells did not substantially repopulate the airway, their administration resulted in increased host ciliated cells, better preservation of airway epithelium, reduction of inflammatory cells, and an increase in animal survival time. Administration of CCSP(+) BMC is beneficial after permanent ablation of lung Clara cells by increasing bronchial epithelial repair. Therefore, CCSP(+) BMC could be important for treatment of lung diseases where airways re-epithelialization is compromised.

Indexed as

Re-EpithelializationAnimalsBone Marrow CellsBronchiolesCell LineCell ProliferationEpithelial CellsFemaleImmunohistochemistryIn Situ Hybridization, FluorescenceLung DiseasesMaleMiceMice, TransgenicPromoter Regions, GeneticRespiratory SystemThymidine KinaseUteroglobin

Identifiers

PMID23609017
PMCPMC3677308
OpenAlexW2087706594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.