Evidence map›Paper›PMID 38332381›Full record

ArticleMolecular biology reports2024

MiR129-5p-loaded exosomes suppress seizure-associated neurodegeneration in status epilepticus model mice by inhibiting HMGB1/TLR4-mediated neuroinflammation.

Tengfei Liu, Haiyan Liu, Siyi Xue, Lijie Xiao, Jing Xu, Shuyan Tong, Xiu'e Wei

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 12 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

7 authors at 1 institution in 1 country.

Tengfei Liu *Department of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Haiyan Liu *Department of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Siyi XueSchool of Medical Imaging, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.
Lijie XiaoDepartment of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Jing XuDepartment of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Shuyan TongDepartment of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Xiu'e WeiDepartment of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China. 523038924@qq.com.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation contributes to both epileptogenesis and the associated neurodegeneration, so regulation of inflammatory signaling is a potential strategy for suppressing epilepsy development and pathological progression. Exosomes are enriched in microRNAs (miRNAs), considered as vital communication tools between cells, which have been proven as potential therapeutic method for neurological disease. Here, we investigated the role of miR129-5p-loaded mesenchymal stem cell (MSC)-derived exosomes in status epilepticus (SE) mice model.

methodsMice were divided into four groups: untreated control (CON group), kainic acid (KA)-induced SE groups (KA group), control exosome injection (KA + Exo-con group), miR129-5p-loaded exosome injection (KA + Exo-miR129-5p group). Hippocampal expression levels of miR129-5p, HMGB1, and TLR4 were compared among groups. Nissl and Fluoro-jade B staining were conducted to evaluate neuronal damage. In addition, immunofluorescence staining for IBA-1 and GFAP was performed to assess glial cell activation, and inflammatory factor content was determined by ELISA. Hippocampal neurogenesis was assessed by BrdU staining.

resultsThe expression of HMGB1 was increased after KA-induced SE and peaking at 48 h, while hippocampal miR129-5p expression decreased in SE mice. Exo-miR129-5p injection reversed KA-induced upregulation of hippocampal HMGB1 and TLR4, alleviated neuronal damage in the hippocampal CA3, reduced IBA-1 + and GFAP + staining intensity, suppressed SE-associated increases in inflammatory factors, and decreased BrdU + cell number in dentate gyrus.

conclusionsExosomes loaded with miR129-5p can protect neurons against SE-mediated degeneration by inhibiting the pro-inflammatory HMGB1/TLR4 signaling axis.

Indexed as

ExosomesHMGB1 ProteinMicroRNAsStatus EpilepticusAnimalsBromodeoxyuridineHippocampusKainic AcidMiceNeuroinflammatory DiseasesSeizuresToll-Like Receptor 4BromodeoxyuridineHMGB1 ProteinHMGB1 protein, mouseKainic AcidMicroRNAsMIRN129 microRNA, mouseTlr4 protein, mouseToll-Like Receptor 4ExosomeKainic acidmiR129-5pNeuroinflammationStatus epilepticus

Identifiers

PMID38332381
PMCPMC10853309
OpenAlexW4391637754

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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.