Evidence map›Paper›PMID 36870962›Full record

ArticleCellular & molecular biology letters2023

Exosomal Mir-3613-3p derived from oxygen-glucose deprivation-treated brain microvascular endothelial cell promotes microglial M1 polarization.

Mengqi Zhang, Qian Wu, Mimi Tang, Zhuohui Chen, Haiyue Wu

Open access · goldAbstract readLetter
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  7. Migrasomes in Ischemic Stroke: Molecular Landscape and Pathophysiological Impact.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

5 authors at 3 institutions in 1 country.

Mengqi ZhangDepartment of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008, Hunan, China. zhangmengqi8912@163.com.
Qian WuDepartment of Neurology, First Affiliated Hospital, Kunming Medical University, Kunming, 650032, China.
Mimi TangDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, 410008, China.
Zhuohui ChenDepartment of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008, Hunan, China.
Haiyue WuDepartment of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008, Hunan, China.
Xiangya Hospital Central South University · CNCentral South University · CNFirst Affiliated Hospital of Kunming Medical University · CN

Funding

National Natural Science Foundation of China No. 81501025Natural Science Foundations for Excellent Young Scholars of Hunan Province No.2021JJ20095Natural Science Foundations of Hunan Province No.2020JJ4134Research Project on Education and Teaching Innovation of Central South University 2021jy145the Key Research and Development Program of Hunan Province No. 2020SK2063
6 · The paper itself

Abstract

backgroundBrain microvascular endothelial cell (BMEC) injury can affect neuronal survival by modulating immune responses through the microenvironment. Exosomes are important vehicles of transport between cells. However, the regulation of the subtypes of microglia by BMECs through the exosome transport of microRNAs (miRNAs) has not been established.

methodsIn this study, exosomes from normal and oxygen-glucose deprivation (OGD)-cultured BMECs were collected, and differentially expressed miRNAs were analyzed. BMEC proliferation, migration, and tube formation were analyzed using MTS, transwell, and tube formation assays. M1 and M2 microglia and apoptosis were analyzed using flow cytometry. miRNA expression was analyzed using real-time polymerase chain reaction (RT-qPCR), and IL-1β, iNOS, IL-6, IL-10, and RC3H1 protein concentrations were analyzed using western blotting.

resultsWe found that miR-3613-3p was enriched in BMEC exosome by miRNA GeneChip assay and RT-qPCR analysis. miR-3613-3p knockdown enhanced cell survival, migration, and angiogenesis in the OGD-treated BMECs. In addition, BMECs secrete miR-3613-3p to transfer into microglia via exosomes, and miR-3613-3p binds to the RC3H1 3' untranslated region (UTR) to reduce RC3H1 protein levels in microglia. Exosomal miR-3613-3p promotes microglial M1 polarization by inhibiting RC3H1 protein levels. BMEC exosomal miR-3613-3p reduces neuronal survival by regulating microglial M1 polarization.

conclusionsmiR-3613-3p knockdown enhances BMEC functions under OGD conditions. Interfering with miR-3613-3p expression in BMSCs reduced the enrichment of miR-3613-3p in exosomes and enhanced M2 polarization of microglia, which contributed to reduced neuronal apoptosis.

Indexed as

ExosomesMicrogliaBrainEndothelial CellsGlucoseGlucoseBrain microvascular endothelial cellExosomeIschemic strokeMacrophageNeuron

Identifiers

PMID36870962
PMCPMC9985860
OpenAlexW4323072945

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.