Evidence map›Paper›PMID 27410685›Full record

ArticlePloS one2016

Pivotal Role of Carbohydrate Sulfotransferase 15 in Fibrosis and Mucosal Healing in Mouse Colitis.

Kenji Suzuki, Somasundaram Arumugam, Junji Yokoyama, Yusuke Kawauchi, Yutaka Honda, Hiroki Sato, Yutaka Aoyagi, Shuji Terai, Kazuichi Okazaki, Yasuo Suzuki and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
8.2field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Identification of Ferro-Aging-Related Biomarkers for Ulcerative Colitis Through Integrated Machine Learning, Single-Cell Analysis, and Spatial Transcriptomics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  15. Emerging therapeutic options in inflammatory bowel disease.World journal of gastroenterology · 2021
    Review
  16. Article
  17. Mouse Models of Intestinal Fibrosis.Methods in molecular biology (Clifton, N.J.) · 2021
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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

18 authors at 8 institutions in 2 countries.

Kenji SuzukiDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Somasundaram ArumugamDepartment of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Science, Niigata city, Niigata, Japan.
Junji YokoyamaDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Yusuke KawauchiDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Yutaka HondaDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Hiroki SatoDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Yutaka AoyagiDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Shuji TeraiDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Kazuichi OkazakiThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi city, Osaka, Japan.
Yasuo SuzukiInternal Medicine, Toho University, Sakura Medical Center, Sakura city, Chiba, Japan.
Shuji MizumotoDepartment of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Nagoya city, Aichi, Japan.
Kazuyuki SugaharaDepartment of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Nagoya city, Aichi, Japan.
Raja AtreyaDepartment of Medicine 1, University of Erlangen-Nürnberg, Erlangen, Bavaria, Germany.
Markus F NeurathDepartment of Medicine 1, University of Erlangen-Nürnberg, Erlangen, Bavaria, Germany.
Kenichi WatanabeDepartment of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Science, Niigata city, Niigata, Japan.
Taishi HashiguchiStelic Institute & Co., Inc., Minato City, Tokyo, Japan.
Hiroyuki YoneyamaStelic Institute & Co., Inc., Minato City, Tokyo, Japan.
Hitoshi AsakuraDepartment of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata city, Niigata, Japan.
Niigata University Medical and Dental Hospital · JPFriedrich-Alexander-Universität Erlangen-Nürnberg · DENiigata University of Pharmacy and Applied Life Sciences · JPStelic Institute (Japan) · JPHokkaido University · JPKansai Medical University · JPMeijo University · JPToho University Medical Center Sakura Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of mucosal healing (MH) is an important treatment goal in inflammatory bowel disease (IBD). Although the molecular mechanisms underlying MH in IBD is not fully explored, local fibrosis would contribute to interfere mucosal repair. Carbohydrate sulfotransferase 15 (CHST15), which catalyzes sulfation of chondroitin sulfate to produce rare E-disaccharide units, is a novel mediator to create local fibrosis. Here we have used siRNA-based approach of silencing CHST15 in dextran sulfate sodium (DSS) induced colitis in mice, human colon fibroblasts and cancer cell lines. In a DSS-induced acute colitis model, CHST15 siRNA reduced CHST15 mRNA in the colon, serum IL-6, disease activity index (DAI) and accumulation of F4/80+ macrophages and ER-TR7+ fibroblasts, while increased Ki-67+ epithelial cells. In DSS-induced chronic colitis models, CHST15 siRNA reduced CHST15 mRNA in the colon, DAI, alpha-smooth muscle actin+ fibroblasts and collagen deposition, while enhanced MH as evidenced by reduced histological and endoscopic scores. We also found that endoscopic submucosal injection achieved effective pancolonic delivery of CHST15 siRNA in mice. In human CCD-18 Co cells, CHST15 siRNA inhibited the expression of CHST15 mRNA and selectively reduced E-units, a specific product biosynthesized by CHST15, in the culture supernatant. CHST15 siRNA significantly suppressed vimentin in both TGF-ß-stimulated CCD18-Co cells and HCT116 cells while up-regulated BMP7 and E-cadherin in HCT116 cells. The present study demonstrated that blockade CHST15 represses colonic fibrosis and enhances MH partly though reversing EMT pathway, illustrating a novel therapeutic opportunity to refractory and fibrotic lesions in IBD.

Indexed as

Acute DiseaseAnimalsCarbohydrate SulfotransferasesColitisColonEpithelial-Mesenchymal TransitionFemaleFibroblastsFibrosisGene Expression RegulationGene SilencingHumansIntestinal MucosaMiceMice, Inbred C57BLRNA, Small InterferingCarbohydrate SulfotransferasesRNA, Small InterferingSulfotransferases

Identifiers

PMID27410685
PMCPMC4943596
OpenAlexW2464641366

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.