Evidence map›Paper›PMID 27077118›Full record

ArticleEBioMedicine2016

Epithelial Cell-Derived a Disintegrin and Metalloproteinase-17 Confers Resistance to Colonic Inflammation Through EGFR Activation.

Masayuki Shimoda, Keisuke Horiuchi, Aya Sasaki, Tetsuya Tsukamoto, Koji Okabayashi, Hirotoshi Hasegawa, Yuko Kitagawa, Yasunori Okada

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Proteases in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. ACE2 contributes to the maintenance of mouse epithelial barrier function.Biochemical and biophysical research communications · 2020
    Article
  18. ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation.International journal of molecular sciences · 2020
    Review
  19. Review
  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

8 authors at 2 institutions in 1 country.

Masayuki ShimodaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Keisuke HoriuchiDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo, Japan.
Aya SasakiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Tetsuya TsukamotoDepartment of Diagnostic Pathology, Fujita Health University School of Medicine, Aichi, Japan.
Koji OkabayashiDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Hirotoshi HasegawaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yuko KitagawaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yasunori OkadaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan; Department of Pathophysiology for Locomotive and Neoplastic Diseases, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Keio University · JPFujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial regeneration is a key process for the recovery from ulcerative colitis (UC). Here we demonstrate that a disintegrin and metalloproteinase-17 (ADAM17), a main sheddase for tumor necrosis factor (TNF)-α, is essential for defensive epithelial properties against UC by promoting epithelial cell growth and goblet cell differentiation in mouse and human. Mice with systemic deletion of Adam17 developed severe dextran sulfate sodium-induced colitis when compared to mice with myeloid cell Adam17 deletion or control littermates. ADAM17 was predominantly expressed by regenerating epithelia in control mice, and its loss or inhibition attenuated epidermal growth factor receptor (EGFR) activation, epithelial proliferation, mucus production and barrier functions. Conversely, ectopic EGFR stimulation promoted epithelial regeneration thereby partially rescuing the severe colitis caused by ADAM17 deficiency. In UC patients, epithelial ADAM17 expression positively correlated with both cell proliferation and goblet cell number. These findings suggest that maintaining ADAM17-EGFR epithelial signaling is necessary for the recovery from UC and would be beneficial to therapeutic strategies targeting ADAM17-mediated TNF-α shedding.

Indexed as

ADAM17 ProteinAnimalsCell ProliferationColitis, UlcerativeColonDextran SulfateDisease Models, AnimalEpithelial CellsErbB ReceptorsGene Expression RegulationGoblet CellsHumansInflammationMiceSignal TransductionTumor Necrosis Factor-alphaADAM17 ProteinAdam17 protein, mouseDextran SulfateEGFR protein, mouseErbB ReceptorsTumor Necrosis Factor-alphaADAM, a disintegrin and metalloproteinaseA disintegrin and metalloproteinase 17 (ADAM17)BrdU, bromodeoxyuridineDSS, dextran sulfate sodiumEGF, epidermal growth factorEGFR, epidermal growth factor receptorEpidermal growth factor receptor (EGFR)Epithelial barrierGoblet cellIBD, inflammatory bowel diseaseMAPK, mitogen activated protein kinaseMMP, matrix metalloproteinasePCNA, proliferation cell nuclear antigenpEGFR, phosphorylated EGFRPI3K, phosphatidylinositol 3-kinasepIpC, polyinosinic–polycytidylic acidRT-qPCR, real-time quantitative PCRSTAT3, signal transducer and activator of transcription 3TACE, tumor necrosis factor-α converting enzymeTGF, transforming growth factorTGM, transglutaminaseTNF, tumor necrosis factorUC, ulcerative colitisUlcerative colitis

Identifiers

PMID27077118
PMCPMC4816818
OpenAlexW2257966482

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.