Evidence map›Paper›PMID 34215174›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

MSCs‑derived exosomes attenuate ischemia-reperfusion brain injury and inhibit microglia apoptosis might via exosomal miR-26a-5p mediated suppression of CDK6.

Chang Cheng, Xiuying Chen, Yuhan Wang, Wenchao Cheng, Xuzheng Zuo, Weiju Tang, Wen Huang

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.1field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 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.

Chang ChengDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Xiuying ChenDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Yuhan WangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Wenchao ChengDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Xuzheng ZuoDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Weiju TangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China.
Wen HuangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), No. 188 Xinqiaozheng Street, Chongqing, 400038, People's Republic of China. WenHuangChongqing@163.com.ORCID 0000-0002-0822-2690
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to explore the role of mesenchymal stromal cells (MSCs)-derived exosomes (MSCs-Exo) in the cerebral ischemia-reperfusion (I/R) injury.

methodsExosomes were isolated from MSCs of adult C57BL/6J mice by the gradient centrifugation method. The expression of miR-26a-5p and CDK6 in MSCs-Exo and mice brain tissues were evaluated by qRT-PCR and western blot. miR-26a-5p mimics and miR-NC were transfected into MSCs, and exosomes were isolated from the MSCs stably expressing miR-26a-5p. Then MSCs-Exo-miR-26a-5p mimics or MSCs-Exo-miR-NC was injected into mice through the tail vein, or added into medium to stimulate BV-2 cells. Cell viability was evaluated by CCK-8 assay. Cell apoptosis was detected by flow cytometry. The apoptosis in brain tissues was evaluated by TUNEL staining assay. Bioinformatics analysis and luciferase reporter assay were performed to determine the binding relationship between miR-26a-5p and CDK6.

resultsmiR-26a-5p was downregulated and CDK6 was upregulated in MSCs-Exo of MCAO-mice and OGD-induced MSCs. MSCs-Exo-miR-26a-5p mimics significantly reduced cell apoptosis of OGD-injured BV-2 cells. MSCs-Exo-miR-26a-5p mimics significantly reduced the infarct volume of MCAO-induced mice. Luciferase reporter assay revealed that CDK-6 was a target of miR-26a-5p. In addition, MSCs-Exo-miR-26a-5p mimics significantly decreased the expression of CDK6 in both OGD-induced BV-2 cells and the brain tissues of MCAO-treated mice.

conclusionOur results indicated that MSCs‑Exo attenuated I/R injury in mice by inhibiting microglia apoptosis might via exosomal miR-26a-5p mediated suppression of CDK6. Our study shed light on the application of MSC-Exo as a potential therapeutic tool for cerebral I/R injury.

Indexed as

AnimalsApoptosisBiomarkersBrainCyclin-Dependent Kinase 6Disease Models, AnimalDisease SusceptibilityExosomesGene Expression RegulationMesenchymal Stem CellsMiceMicrogliaMicroRNAsReperfusion InjuryRNA InterferenceBiomarkersCdk6 protein, mouseCyclin-Dependent Kinase 6MicroRNAsMirn26 microRNA, mouseCDK6ExosomesIschemia–reperfusion injuryMesenchymal stromal cellsmiR-26a-5p

Identifiers

PMID34215174
PMCPMC8254277
OpenAlexW3105855091

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.