Evidence map›Paper›PMID 32331514›Full record

ArticleJournal of neuroinflammation2020

Eicosapentaenoic acid prevents the progression of intracranial aneurysms in rats.

Yu Abekura, Isao Ono, Akitsugu Kawashima, Katsumi Takizawa, Hirokazu Koseki, Haruka Miyata, Kampei Shimizu, Mieko Oka, Mika Kushamae, Susumu Miyamoto and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 15 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

13 authors at 8 institutions in 1 country.

Yu AbekuraDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Isao OnoDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Akitsugu KawashimaDepartment of Neurosurgery, Tokyo Women's Medical University Yachiyo Medical Center, Chiba, Japan.
Katsumi TakizawaDepartment of Neurosurgery, Asahikawa Red Cross Hospital, Hokkaido, Japan.
Hirokazu KosekiDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Haruka MiyataDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Kampei ShimizuDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Mieko OkaDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Mika KushamaeDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan.
Susumu MiyamotoDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroharu KataokaDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akira IshiiDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tomohiro AokiDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, 564-8565, Japan. tomoaoki@ncvc.go.jp.
Kyoto University · JPJapan Agency for Medical Research and Development · JPJapanese Red Cross Asahikawa Hospital · JPNational Cerebral and Cardiovascular Center · JPShowa University · JPThe Jikei University Hospital · JPTokyo Women's Medical University · JPTokyo Women's Medical University Yachiyo Medical Center

Funding

Core Research for Evolutional Science and Technology on Mechanobiology from the Japan Agency for Medical Research and Development 19gm0810006Core Research for Evolutional Science and Technology on Mechanobiology from the Japan Agency for Medical Research and Development JP18gm0810006
6 · The paper itself

Abstract

backgroundAs subarachnoid hemorrhage due to rupture of an intracranial aneurysm (IA) has quite a poor outcome despite of an intensive medical care, development of a novel treatment targeting unruptured IAs based on the correct understanding of pathogenesis is mandatory for social health.

methodsUsing previously obtained gene expression profile data from surgically resected unruptured human IA lesions, we selected G-protein coupled receptor 120 (GPR120) as a gene whose expression is significantly higher in lesions than that in control arterial walls. To corroborate a contribution of GPR120 signaling to the pathophysiology, we used an animal model of IAs and examine the effect of a GPR120 agonist on the progression of the disease. IA lesion was induced in rats through an increase of hemodynamic stress achieved by a one-sided carotid ligation and induced hypervolemia. Eicosapentaenoic acid (EPA) was used as an agonist for GPR120 in this study and its effect on the size of IAs, the thinning of media, and infiltration of macrophages in lesions were examined.

resultEPA administered significantly suppressed the size of IAs and the degenerative changes in the media in rats. EPA treatment also inhibited infiltration of macrophages, a hallmark of inflammatory responses in lesions. In in vitro experiments using RAW264.7 cells, pre-treatment of EPA partially suppressed lipopolysaccharide-induced activation of nuclear factor-kappa B and also the transcriptional induction of monocyte chemoattractant protein 1 (MCP-1), a major chemoattractant for macrophages to accumulate in lesions. As a selective agonist of GPR120, TUG-891, could reproduce the effect of EPA in RAW264.7 cells, EPA presumably acted on this receptor to suppress inflammatory responses. Consistently, EPA remarkably suppressed MCP-1 expression in lesions, suggesting the in vivo relevance of in vitro studies.

conclusionsThese results combined together suggest the potential of the medical therapy targeting GPR120 or using EPA to prevent the progression of IAs.

Indexed as

AnimalsBrainDisease ProgressionEicosapentaenoic AcidHumansIntracranial AneurysmMaleMiceRatsRats, Sprague-DawleyRAW 264.7 CellsReceptors, G-Protein-CoupledEicosapentaenoic AcidReceptors, G-Protein-CoupledEicosapentaenoic acidGPR120Intracranial aneurysm

Identifiers

PMID32331514
PMCPMC7181479
OpenAlexW3018418630

What OpenQuestion holds

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LicenceCC BY
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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.