Evidence map›Paper›PMID 25687338›Full record

ArticleScientific reports2015

Impact of Sox9 dosage and Hes1-mediated Notch signaling in controlling the plasticity of adult pancreatic duct cells in mice.

Shinichi Hosokawa, Kenichiro Furuyama, Masashi Horiguchi, Yoshiki Aoyama, Kunihiko Tsuboi, Morito Sakikubo, Toshihiko Goto, Koji Hirata, Wataru Tanabe, Yasuhiro Nakano and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  9. Article
  10. Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2017
    Review
  11. Review
  12. Article
  13. Review
  14. Notch Signaling in Pancreatic Development.International journal of molecular sciences · 2015
    Review
  15. 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

14 authors at 2 institutions in 1 country.

Shinichi Hosokawa1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Kenichiro Furuyama1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Masashi Horiguchi1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Yoshiki Aoyama1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Kunihiko Tsuboi1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Morito Sakikubo1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Toshihiko Goto1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Koji Hirata1] Department of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan [2] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Wataru Tanabe1] Department of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan [2] Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yasuhiro NakanoDepartment of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Haruhiko AkiyamaDepartment of Orthopaedics, Gifu University, Gifu, Japan.
Ryoichiro KageyamaInstitute for Virus Research, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shinji UemotoDepartment of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoshiya KawaguchiDepartment of Clinical Application, Center for iPS cell Research and Application, Kyoto University, Kyoto, Japan.
Kyoto University · JPGifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the adult pancreas, there has been a long-standing dispute as to whether stem/precursor populations that retain plasticity to differentiate into endocrine or acinar cell types exist in ducts. We previously reported that adult Sox9-expressing duct cells are sufficiently plastic to supply new acinar cells in Sox9-IRES-CreERT2 knock-in mice. In the present study, using Sox9-IRES-CreERT2 knock-in mice as a model, we aimed to analyze how plasticity is controlled in adult ducts. Adult duct cells in these mice express less Sox9 than do wild-type mice but Hes1 equally. Acinar cell differentiation was accelerated by Hes1 inactivation, but suppressed by NICD induction in adult Sox9-expressing cells. Quantitative analyses showed that Sox9 expression increased with the induction of NICD but did not change with Hes1 inactivation, suggesting that Notch regulates Hes1 and Sox9 in parallel. Taken together, these findings suggest that Hes1-mediated Notch activity determines the plasticity of adult pancreatic duct cells and that there may exist a dosage requirement of Sox9 for keeping the duct cell identity in the adult pancreas. In contrast to the extended capability of acinar cell differentiation by Hes1 inactivation, we obtained no evidence of islet neogenesis from Hes1-depleted duct cells in physiological or PDL-induced injured conditions.

Indexed as

Cell PlasticityGene DosageSignal TransductionAge FactorsAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationGene ExpressionHomeodomain ProteinsMiceMice, TransgenicModels, BiologicalPancreatic DuctsReceptors, NotchSOX9 Transcription FactorTranscription Factor HES-1Basic Helix-Loop-Helix ProteinsHes1 protein, mouseHomeodomain ProteinsReceptors, NotchSOX9 Transcription FactorTranscription Factor HES-1transcription factor PTF1Transcription Factors

Identifiers

PMID25687338
PMCPMC4330537
OpenAlexW1976829109

What OpenQuestion holds

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LicenceCC BY
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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.