Evidence map›Paper›PMID 31221118›Full record

ArticleBMC pulmonary medicine2019

Increased extracellular vesicle miRNA-466 family in the bronchoalveolar lavage fluid as a precipitating factor of ARDS.

Sotaro Shikano, Yasuhiro Gon, Shuichiro Maruoka, Tetsuo Shimizu, Yutaka Kozu, Yuko Iida, Mari Hikichi, Mai Takahashi, Shinichi Okamoto, Kota Tsuya and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  7. A Review of Extracellular Vesicles in COVID-19 Diagnosis, Treatment, and Prevention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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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

13 authors at 1 institution in 1 country.

Sotaro ShikanoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Yasuhiro GonDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Shuichiro MaruokaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Tetsuo ShimizuDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Yutaka KozuDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Yuko IidaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Mari HikichiDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Mai TakahashiDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Shinichi OkamotoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Kota TsuyaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Asami FukudaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Kenji MizumuraDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan. mizumura.kenji@nihon-u.ac.jp.ORCID http://orcid.org/0000-0001-8532-9670
Shu HashimotoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Nihon University · JP

Funding

Japan Society for the Promotion of Science 15K09196Strategic Research Foundation for Private Universities from the Ministry of Education, Culture, Sports, Science and Technology of Japan S1511014
6 · The paper itself

Abstract

backgroundAcute respiratory distress syndrome (ARDS) is a life-threatening disease; however, its treatment has not yet been fully established. The progression of ARDS is considered to be mediated by altered intercellular communication between immune and structural cells in the lung. One of several factors involved in intercellular communication is the extracellular vesicle (EV). They act as carriers of functional content such as RNA molecules, proteins, and lipids and deliver cargo from donor to recipient cells. EVs have been reported to regulate the nucleotide-binding oligomerization like receptor 3 (NLRP3) inflammasome. This has been identified as the cellular machinery responsible for activating inflammatory processes, a key component responsible for the pathogenesis of ARDS.

methodsHere, we provide comprehensive genetic analysis of microRNAs (miRNAs) in EVs, demonstrating increased expression of the miRNA-466 family in the bronchoalveolar lavage fluid of a mouse ARDS model.

resultsTransfection of bone marrow-derived macrophages (BMDMs) with miRNA-466 g and 466 m-5p resulted in increased interleukin-1 beta (IL-1β) release after LPS and ATP treatment, which is an established in vitro model of NLRP3 inflammasome activation. Moreover, LPS-induced pro-IL-1β expression was accelerated by miRNA-466 g and 466 m-5p in BMDMs.

conclusionsThese findings imply that miRNA-466 family molecules are secreted via EVs into the airways in an ARDS model, and this exacerbates inflammation through the NLRP3 inflammasome. Our results suggest that the NLRP3 inflammasome pathway, regulated by extracellular vesicle miRNA, could act as a therapeutic target for ARDS.

Indexed as

AnimalsBronchoalveolar Lavage FluidDisease Models, AnimalExtracellular VesiclesInflammasomesInflammationInterleukin-1betaLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsNLR Family, Pyrin Domain-Containing 3 ProteinPrecipitating FactorsRespiratory Distress SyndromeInflammasomesInterleukin-1betaLipopolysaccharidesMicroRNAsMirn466 microRNA, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseARDSExtracellular vesiclesmiRNANLRP3 inflammasome

Identifiers

PMID31221118
PMCPMC6584994
OpenAlexW2949104422

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.