Evidence map›Paper›PMID 32393354›Full record

ArticleMolecular brain2020

Altered behavior in mice overexpressing soluble ST2.

Motoshi Kikuchi, Kenkichi Takase, Morisada Hayakawa, Hiroko Hayakawa, Shin-Ichi Tominaga, Tsukasa Ohmori

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  6. IL-33 in Mental Disorders.Medicina (Kaunas, Lithuania) · 2021
    Review
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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

6 authors at 2 institutions in 1 country.

Motoshi KikuchiLaboratory of Natural History, Jichi Medical University School of Medicine, Tochigi, Japan.
Kenkichi TakaseLaboratory of Psychology, Jichi Medical University School of Medicine, Tochigi, Japan. kenkichi.takase@jichi.ac.jp.
Morisada HayakawaDepartment of Biochemistry, Jichi Medical University School of Medicine, Tochigi, Japan.
Hiroko HayakawaDepartment of Biochemistry, Jichi Medical University School of Medicine, Tochigi, Japan.
Shin-Ichi TominagaDepartment of Biochemistry, Jichi Medical University School of Medicine, Tochigi, Japan.
Tsukasa OhmoriDepartment of Biochemistry, Jichi Medical University School of Medicine, Tochigi, Japan.
Jichi Medical University · JPJapan Association for Development of Community Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psychoneuroimmunological studies have clearly demonstrated that both cellular and humoral immunity are related to major depression. Soluble ST2 is regarded as a key molecule regulating immune system as well as cell proliferation. Indeed, soluble ST2 is reported to reduce IL-33-induced IL-6 and TNF-α production in macrophages and IL-33-induced IL-5 and IL-13 production in type 2 innate lymphoid cells. Elevated serum concentrations of soluble ST2 have been reported in patients with neuropsychiatric disorders, suggesting pathophysiological roles of soluble ST2 in behavioral phenotypes. Nevertheless, the relation between soluble ST2 and depressive behavior remain to be uncovered. To complement this point, we performed broad behavioral phenotyping, utilizing transgenic mice with a high concentration of serum ST2 in the present study. Soluble ST2 overexpression mice (ST2 Tg mice) were generated on a C3H/HeJ background. ST2 Tg mice crossed onto the BALB/c genetic background were used. Before starting tests, each mouse was observed in a clean cage for a general health check and neurological screening tests. In Experiment I, comprehensive behavioral phenotyping was performed to reveal the role of soluble ST2 on sensorimotor functions, anxiety-like behaviors, depression-like behaviors, social behaviors, and learning and memory functions. In Experiment II, to confirm the role of soluble ST2 on depression-like behaviors, a depression test battery (two bottle choice test, forced swimming test, and tail suspension test) was applied. The general health check indicated good general health and normal gross appearance for ST2 Tg mice. Further, the neurological reflexes of all the mice were normal. We found that soluble ST2 overexpression resulted in decreased social interaction. Moreover, depression-like behaviors of ST2 Tg mice were observed in two well-established behavioral paradigms, the forced swimming test and the tail suspension test. Nevertheless, hedonic reaction to sucrose was observed in ST2 Tg mice similar to WT mice. These results suggest the depression in the ST2 Tg mice. In conclusion, through a series of experiments, we established the animal model for assessing role of soluble ST2 in neuropsychiatric disorders, and revealed the possible involvement of soluble ST2 in depressive behavior.

Indexed as

MemoryAnimalsAnxietyBehavior, AnimalBehavior Rating ScaleDepressionDisease Models, AnimalInterleukin-1 Receptor-Like 1 ProteinLearningMaze LearningMiceMice, Inbred BALB CMice, Inbred C3HMice, TransgenicMotor ActivitySocial BehaviorIl1rl1 protein, mouseInterleukin-1 Receptor-Like 1 ProteinDepressionForced swimming testMouseSoluble ST2Tail suspension test

Identifiers

PMID32393354
PMCPMC7216579
OpenAlexW3026299453

What OpenQuestion holds

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LicenceCC BY
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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.