Evidence map›Paper›PMID 30136196›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2018

Lysosomal membrane permeabilization causes secretion of IL-1β in human vascular smooth muscle cells.

Hiroaki Ono, Ryo Ohta, Yuri Kawasaki, Akira Niwa, Hidetoshi Takada, Tatsutoshi Nakahata, Shouichi Ohga, Megumu K Saito

Open access · hybridAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Hiroaki OnoDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
Ryo OhtaDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
Yuri KawasakiDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
Akira NiwaDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
Hidetoshi TakadaDepartment of Perinatal and Pediatric Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Tatsutoshi NakahataDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
Shouichi OhgaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Megumu K SaitoDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan. msaito@cira.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0001-8813-3614
Kyoto University · JPKyushu University · JP

Funding

Japan Agency for Medical Research and Development 14525849
6 · The paper itself

Abstract

objectiveIL-1β secretion by the inflammasome is strictly controlled and requires two sequential signals: a priming signal and an activating signal. Lysosomal membrane permeabilization (LMP) plays a critical role in the regulation of NLRP3 inflammasome, and generally acts as an activating signal. However, the role of LMP controlling NLRP3 inflammasome activation in human vascular smooth muscle cells (hVSMCs) is not well defined.

methodsLMP was induced in hVSMCs by Leu-Leu-O-methyl ester. Cathepsin B was inhibited by CA-074 Me. Cytokine release, mRNA, and protein were quantified by enzyme-linked immunosorbent assay, quantitative PCR, and Western blot, respectively. NF-κB activity was analyzed by immunostaining of the NF-κB p65 nuclear translocation and using the dual-luciferase reporter assay system.

resultsLMP had both priming and activating roles, causing an upregulation of proIL-1β and NLRP3 and the secretion of mature IL-1β from unprimed hVSMCs. LMP activated the canonical NF-κB pathway. The priming effect of LMP was inhibited by CA-074 Me, indicating an upstream role of cathepsin B.

conclusionsThese data support a novel role of LMP as a single stimulus for the secretion of IL-1β from hVSMCs, implying the possibility that hVSMCs are an important initiator of the sterile inflammatory response caused by lysosomal disintegration.

Indexed as

Cells, CulturedCytokinesHumansInflammasomesLysosomesMonocytesMyocytes, Smooth MuscleNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesCytokinesInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesCathepsin BHuman vascular smooth muscle cells (hVSMCs)InflammasomeLysosomal membrane permeabilization (LMP)NF-κB

Identifiers

PMID30136196
PMCPMC6133165
OpenAlexW2888422553

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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.