Evidence map›Paper›PMID 33002329›Full record

ArticleJournal of cellular and molecular medicine2020

CircHivep2 contributes to microglia activation and inflammation via miR-181a-5p/SOCS2 signalling in mice with kainic acid-induced epileptic seizures.

Gao Xiaoying, Mian Guo, Liu Jie, Zhu Yanmei, Cui Ying, Shu Shengjie, Gou Haiyan, Sun Feixiang, Qi Sihua, Sun Jiahang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 50 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

10 authors at 1 institution in 1 country.

Gao XiaoyingDepartment of Anesthesiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Mian GuoDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Liu JieDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhu YanmeiDepartment of Radiology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Cui YingDepartment of Neurology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Shu ShengjieDepartment of Imageology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Gou HaiyanDepartment of Radiology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Sun FeixiangDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Qi SihuaDepartment of Anesthesiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Sun JiahangDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID 0000-0002-7945-0244
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a chronic brain disease characterized by recurrent seizures. Circular RNA (circRNA) is a novel family of endogenous non-coding RNAs that have been proposed to regulate gene expression. However, there is a lack of data on the role of circRNA in epilepsy. In this study, the circRNA profiles were evaluated by microarray analysis. In total, 627 circRNAs were up-regulated, whereas 892 were down-regulated in the hippocampus in mice with kainic acid (KA)-induced epileptic seizures compared with control. The expression of circHivep2 was significantly down-regulated in hippocampus tissues of mice with KA-induced epileptic seizures and BV-2 microglia cells upon KA treatment. Bioinformatics analysis predicted that circHivep2 interacts with miR-181a-5p to regulate SOCS2 expression, which was validated using a dual-luciferase reporter assay. Moreover, overexpression of circHivep2 significantly inhibited KA-induced microglial activation and the expression of inflammatory factors in vitro, which was blocked by miR-181a-5p, whereas circHivep2 knockdown further induced microglia cell activation and the release of pro-inflammatory proteins in BV-2 microglia cells after KA treatment. The application of circHivep2+ exosomes derived from adipose-derived stem cells (ADSCs) exerted significant beneficial effects on the behavioural seizure scores of mice with KA-induced epilepsy compared to control exosomes. The circHivep2+ exosomes also inhibited microglial activation, the expression of inflammatory factors, and the miR-181a-5p/SOCS2 axis in vivo. Our results suggest that circHivep2 regulates microglia activation in the progression of epilepsy by interfering with miR-181a-5p to promote SOCS2 expression, indicating that circHivep2 may serve as a therapeutic tool to prevent the development of epilepsy.

Indexed as

AdipocytesAnimalsBiotinylationCell LineDNA-Binding ProteinsEpilepsyExosomesGene Expression ProfilingGene Expression RegulationHippocampusInflammationIn Situ Hybridization, FluorescenceKainic AcidMaleMiceMice, Inbred C57BLDNA-Binding ProteinsHivep2 protein, mouseKainic AcidMicroRNAsmirn181 microRNA, mouseRNA, CircularRNA, Long NoncodingSocs2 protein, mouseSuppressor of Cytokine Signaling Proteinscircular RNAsepilepsyinflammatory responsemicroglia activationmiR-181a-5p

Identifiers

PMID33002329
PMCPMC7701587
OpenAlexW3091368739

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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.