Evidence map›Paper›PMID 20565818›Full record

ArticleBMC gastroenterology2010

Altered expression of a putative progenitor cell marker DCAMKL1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia.

Miho Kikuchi, Hiroshi Nagata, Norihito Watanabe, Hiromitsu Watanabe, Masayuki Tatemichi, Toshifumi Hibi

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. World journal of clinical cases · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Dclk1-expressing tuft cells: critical modulators of the intestinal niche?American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  8. Review
  9. Article
  10. Epithelial Regeneration After Gastric Ulceration Causes Prolonged Cell-Type Alterations.Cellular and molecular gastroenterology and hepatology · 2016
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Recent progress in histochemistry and cell biology.Histochemistry and cell biology · 2012
    Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 5 institutions in 1 country.

Miho KikuchiDepartment of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Hiroshi Nagata
Norihito Watanabe
Hiromitsu Watanabe
Masayuki Tatemichi
Toshifumi Hibi
Keio University · JPHiroshima University · JPkeiyu Hospital · JPShowa University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDoublecortin and calcium/calmodulin-dependent protein kinase-like-1 (DCAMKL1) is a candidate marker for progenitor cells in the gastrointestinal mucosa. Lineage cells in the gastric mucosa are derived from progenitor cells, but this process can be altered after injury. Therefore, we explored DCAMKL1 expression under pathological conditions.

methodsAn immunohistochemical analysis was performed in rat stomach with acute superficial injury, chronic ulcer, intestinal metaplasia and dysplasia.

resultsDCAMKL1 was exclusively expressed in immature quiescent cells in the isthmus of normal fundic glands, where putative progenitor cells are thought to reside. DCAMKL1-positive cells and proliferating cells shed into the lumen after superficial injury and re-appeared during the regenerative process, mainly in the superficial mucosa. In the marginal mucosa around the active ulcer, parietal and chief cells diminished, foveolar hyperplasia was evident, and trefoil factor family 2 (TFF2)/spasmolytic polypeptide-expressing metaplasia (SPEM) emerged at the gland base. DCAMKL1 cells re-emerged in the deep mucosa juxtaposed with SPEM and proliferating cells. In the healing ulcer, the TFF2 cell population expanded and seemed to redifferentiate to chief cells, while proliferating cells and DCAMKL1 cells appeared above and below the TFF2 cells to promote healing. SPEM appeared and PCNA cells increased in the intestinalized mucosa, and DCAMKL1 was expressed in the proximity of the PCNA cells in the deep mucosa. DCAMKL1, PCNA and TFF2 were expressed in different dysplastic cells lining dilated glands near SPEM.

conclusionThe ultrastructural appearance of DCAMKL1-positive cells and the expression patterns of DCAMKL1 in normal and pathological states indicate that the cells belong to a progenitor cell population. DCAMKL1 expression is closely associated with TFF2/SPEM cells after injury. DCAMKL1 cells repopulate close to proliferating, hyperplastic, metaplastic and dysplastic cells, and the progenitor zone shifts according to the pathological circumstances.

Indexed as

Acetic AcidAnimalsBiomarkersCell ProliferationDisease Models, AnimalDoublecortin-Like KinasesDoublecortin ProteinGastric MucosaIntestinal DiseasesMaleMetaplasiaMethylnitronitrosoguanidineProtein Serine-Threonine KinasesRatsRats, WistarRegenerationAcetic AcidBiomarkersDclk1 protein, ratDcx protein, ratDoublecortin-Like KinasesDoublecortin ProteinMethylnitronitrosoguanidineProtein Serine-Threonine KinasesTff2 protein, ratTrefoil Factor-2

Identifiers

PMID20565818
PMCPMC2912238
OpenAlexW2020009452

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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.