Evidence map›Paper›PMID 21377457›Full record

ArticleDevelopmental biology2011

Ascl3 knockout and cell ablation models reveal complexity of salivary gland maintenance and regeneration.

Szilvia Arany, Marcelo A Catalán, Elisa Roztocil, Catherine E Ovitt

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026
    Review
  3. Ascl3The Journal of physiology · 2026
    Article
  4. Article
  5. A mathematical model of ENaC and Slc26a6 regulation by CFTR in salivary gland ducts.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  6. Article
  7. CFTR expression in human salivary gland acinar cells.American journal of physiology. Cell physiology · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Cell signaling regulation in salivary gland development.Cellular and molecular life sciences : CMLS · 2021
    Review
  16. Regenerative Medicine of Epithelia: Lessons From the Past and Future Goals.Frontiers in bioengineering and biotechnology · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Szilvia AranyCenter for Oral Biology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Marcelo A Catalán
Elisa Roztocil
Catherine E Ovitt
University of Rochester · US

Funding

PHYSIOLOGY OF MUCUS-SECRETING SALIVARY GLANDSR01DE008921 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE · 1989 to 2013
$2.9M
Salivary gland precursor cellsR01DE018896 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE · 2009 to 2013
$2.1M
NIDCR NIH HHS R01 DE008921NIDCR NIH HHS R01 DE018896
6 · The paper itself

Abstract

Expression of the transcription factor, Ascl3, marks a population of adult progenitor cells, which can give rise to both acinar and duct cell types in the murine salivary glands. Using a previously reported Ascl3(EGFP-Cre/+) knock-in strain, we demonstrate that Ascl3-expressing cells represent a molecularly distinct, and proliferating population of progenitor cells located in salivary gland ducts. To investigate both the role of the Ascl3 transcription factor, and the role of the cells in which it is expressed, we generated knockout and cell-specific ablation models. Ascl3 knockout mice develop smaller salivary glands than wild type littermates, but secrete saliva normally. They display a lower level of cell proliferation, consistent with their smaller size. In the absence of Ascl3, the cells maintain their progenitor function and continue to generate both acinar and duct cells. To directly test the role of the progenitor cells, themselves, in salivary gland development and regeneration, we used Cre-activated expression of diphtheria toxin (DTA) in the Ascl3-expressing (Ascl3+) cell population, resulting in specific cell ablation of Ascl3+ cells. In the absence of the Ascl3+ progenitor cells, the mice developed morphologically normal, albeit smaller, salivary glands able to secrete saliva. Furthermore, in a ductal ligation model of salivary gland injury, the glands of these mice were able to regenerate acinar cells. Our results indicate that Ascl3+ cells are active proliferating progenitors, but they are not the only precursors for salivary gland development or regeneration. We conclude that maintenance of tissue homeostasis in the salivary gland must involve more than one progenitor cell population.

Indexed as

Adult Stem CellsAnimalsBasic Helix-Loop-Helix ProteinsCell LineageCell ProliferationGene Knockout TechniquesMiceMice, KnockoutMice, TransgenicOrgan SizeRegenerationSalivaSalivary GlandsAscl3 protein, mouseBasic Helix-Loop-Helix Proteins

Identifiers

PMID21377457
PMCPMC3093111
OpenAlexW2026537737

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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.