Evidence map›Paper›PMID 25938626›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2015

Microangiopathy triggers, and inducible nitric oxide synthase exacerbates dextran sulfate sodium-induced colitis.

Hiroki Saijo, Norifumi Tatsumi, Seiji Arihiro, Tomohiro Kato, Masataka Okabe, Hisao Tajiri, Hisashi Hashimoto

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Protective Effect ofJournal of microbiology and biotechnology · 2026
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  18. SLC26A3 (DRA) prevents TNF-alpha-induced barrier dysfunction and dextran sulfate sodium-induced acute colitis.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  19. Evidence-based complementary and alternative medicine : eCAM · 2018
    Article
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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 1 institution in 1 country.

Hiroki Saijo1] Department of Anatomy, The Jikei University School of Medicine, Tokyo, Japan [2] Division of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Norifumi TatsumiDepartment of Anatomy, The Jikei University School of Medicine, Tokyo, Japan.
Seiji ArihiroDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Tomohiro KatoDepartment of Endoscopy, The Jikei University School of Medicine, Tokyo, Japan.
Masataka OkabeDepartment of Anatomy, The Jikei University School of Medicine, Tokyo, Japan.
Hisao Tajiri1] Division of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan [2] Department of Endoscopy, The Jikei University School of Medicine, Tokyo, Japan.
Hisashi HashimotoDepartment of Anatomy, The Jikei University School of Medicine, Tokyo, Japan.
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a representative clinical manifestation of inflammatory bowel disease that causes chronic gastrointestinal tract inflammation. Dextran sulfate sodium (DSS)-induced colitis mice have been used to investigate UC pathogenesis, and in this UC model, disturbance and impairment of the mucosal epithelium have been reported to cause colitis. However, how DSS sporadically breaks down the epithelium remains unclear. In this study, we focused on the colonic microcirculation and myenteric neurons of DSS-induced colitis. Moreover, we examined the potential of myenteric neurons as a target to prevent exacerbation of colitis. Fluorescent angiographic and histopathological studies revealed that DSS administration elicited blood vessel disruption before epithelial disorders appeared. Ischemic conditions in the lamina propria induced inducible nitric oxide synthase (iNOS) expression in myenteric neurons as colitis aggravated. When neuronal activity was inhibited with butylscopolamine, neuronal iNOS expression decreased, and the exacerbation of colitis was prevented. These results suggested that DSS-induced colitis was triggered by microcirculatory disturbance in the mucosa, and that excessive neuronal excitation aggravated colitis. During remission periods of human UC, endoscopic inspection of the colonic microcirculation may enable the early detection of disease recurrence, and inhibition of neuronal iNOS expression may prevent the disease from worsening.

Indexed as

MicrocirculationActinsAnimalsAntibodies, Monoclonal, HumanizedBevacizumabButylscopolammonium BromideCapillariesCapillary PermeabilityColitisColonDextran SulfateDisease Models, AnimalEnteric Nervous SystemHypoxia-Inducible Factor 1, alpha SubunitIntestinal MucosaMaleActinsalpha-smooth muscle actin, mouseAntibodies, Monoclonal, HumanizedBevacizumabButylscopolammonium BromideDextran SulfateHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitNitric Oxide Synthase Type IINos2 protein, mousePeripherinsPlatelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID25938626
OpenAlexW1522804491

What OpenQuestion holds

Textmetadata
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.