Evidence map›Paper›PMID 30092402›Full record

ArticleMolecular therapy. Nucleic acids2018

The Supercarbonate Apatite-MicroRNA Complex Inhibits Dextran Sodium Sulfate-Induced Colitis.

Tadafumi Fukata, Tsunekazu Mizushima, Junichi Nishimura, Daisuke Okuzaki, Xin Wu, Haruka Hirose, Yuhki Yokoyama, Yui Kubota, Kazuya Nagata, Naoto Tsujimura and 11 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Functional assessment of miR‑1291 in colon cancer cells.International journal of oncology · 2022
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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

21 authors at 1 institution in 1 country.

Tadafumi FukataDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Tsunekazu MizushimaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Junichi NishimuraDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Yamadaoka 3-1, Suita City, Osaka, Japan.
Xin WuDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan.
Haruka HiroseDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan.
Yuhki YokoyamaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan.
Yui KubotaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan.
Kazuya NagataDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan.
Naoto TsujimuraDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Akira InoueDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Norikatsu MiyoshiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Naotsugu HaraguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Hidekazu TakahashiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Taishi HataDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Chu MatsudaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Hisako KayamaLaboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Yamadaoka 2-2, Suita City, Osaka, Japan; Laboratory of Mucosal Immunology, WPI Immunology Frontier Research Center, Osaka University, Yamadaoka3-1, Suita City, Osaka, Japan.
Kiyoshi TakedaLaboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Yamadaoka 2-2, Suita City, Osaka, Japan; Laboratory of Mucosal Immunology, WPI Immunology Frontier Research Center, Osaka University, Yamadaoka3-1, Suita City, Osaka, Japan.
Yuichiro DokiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Masaki MoriDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan.
Hirofumi YamamotoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita City, Osaka, Japan; Department of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Yamadaoka 1-7, Suita City, Osaka, Japan. Electronic address: hyamamoto@sahs.med.osaka-u.ac.jp.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of inflammatory bowel disease (IBD) is increasing. Nucleic acid-based medicine has potential as a next-generation treatment, but it is rarely successful with IBD. The aim of this study was to establish a microRNA-based therapy in an IBD model. For this purpose, we used microRNA-29 (miR-29) and a supercarbonate apatite (sCA) nanoparticle as a drug delivery system. Injection of sCA-miR-29a-3p or sCA-miR-29b-3p into mouse tail veins markedly prevented and restored inflammation because of dextran sulfate sodium (DSS)-induced colitis. RNA sequencing analysis revealed that miR-29a and miR-29b could inhibit the interferon-associated inflammatory cascade. Subcutaneous injection of sCA-miR-29b also potently inhibited inflammation, and it efficiently targeted CD11c

Indexed as

dendritic cellsDSS colitismicroRNA-29amicroRNA-29bsupercarbonate apatite

Identifiers

PMID30092402
PMCPMC6083010
OpenAlexW2887726433

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.