Evidence map›Paper›PMID 34435328›Full record

ArticleMolecular neurobiology2021

Circular RNA 0025984 Ameliorates Ischemic Stroke Injury and Protects Astrocytes Through miR-143-3p/TET1/ORP150 Pathway.

Daixuan Zhou, Zhi Huang, Xiaoxi Zhu, Tao Hong, Yuanli Zhao

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  20. The Role of Circular RNAs in Ischemic Stroke.Neurochemical research · 2023
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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.

Daixuan Zhou *Queen Mary College, Nanchang University, Nanchang, 330031, People's Republic of China.
Zhi Huang *School of Basic Medical Science, Guizhou Medical University, Guiyang, 550002, People's Republic of China.
Xiaoxi ZhuKey Laboratory of Endemic and Ethnic Diseases, Ministry of Education, Guizhou Medical University, Guiyang, 550002, People's Republic of China.
Tao HongDepartment of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330029, People's Republic of China. htdoctor2000@sina.com.ORCID http://orcid.org/0000-0002-4125-8011
Yuanli ZhaoDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Nanchang, 100070, People's Republic of China. zhaoyuanli@pkuih.edu.cn.
Guiyang Medical University · CNNanchang University · CNCapital Medical University · CN

Funding

National Natural Science Foundation of China 81860321
6 · The paper itself

Abstract

MiR-143-3p is aberrantly expressed in patients with ischemic stroke and associated with ischemic brain injury. However, the underlying mechanisms are largely unknown. Here, we confirmed circ_0025984 and TET1 as a sponge and target of miR-143-3p, respectively, by luciferase reporter assay. In astrocytes, OGD significantly decreased circ_0025984 and TET1 levels but increased miR-143-3p levels, which was also observed in brains of mice with MCAO. Treatment with miR-143-3p inhibitor or circ_0025984 significantly decreased astrocyte apoptosis and autophagy, as well as cerebral injury and neuron loss in mice with MCAO. Notably, TET1 overexpression decreased astrocyte apoptosis and autophagy and induced promoter hypomethylation and expression of ORP150. Our results demonstrated for the first time that circ_0025984 protects astrocytes from ischemia-induced autophagy and apoptosis by targeting the miR-143-3p/TET1 pathway and might inhibit cerebral injury induced by ischemic stroke. Furthermore, our data revealed the important positive regulation of ORP150 by TET1, which could be associated with its neuroprotective role. Graphical abstract Model for signaling pathway of circ_0025984/miR-143-3p/TET1 inastrocytes cultured under OGD. In astrocytes, circ_0025984 acts as a sponge of miR-143-3p, which directly targets TET1 and decreases its expression (A). After translocatinginto the nucleus, TET1 binds to the promoter of ORP150, converts 5mC into 5hmC,leading to DNA demethylation and increased expression of ORP150 (B). In astrocytescultured under OGD, ER stress is induced and eventually leads to apoptosis andautophagy mediated by ATG7, which is regulated by circ_0025984 via ORP150 andGRP78 (C).

Indexed as

AnimalsApoptosisAstrocytesAstrocytomaAutophagyCell Line, TumorDioxygenasesGene Expression RegulationGenes, ReporterHSP70 Heat-Shock ProteinsHumansInfarction, Middle Cerebral ArteryMaleMicroRNAsMixed Function OxygenasesNerve Tissue ProteinsDioxygenasesHSP70 Heat-Shock ProteinsMicroRNAsMIRN143 microRNA, humanMIRN143 microRNA, ratMixed Function OxygenasesNerve Tissue Proteinsoxygen-regulated proteinsProto-Oncogene ProteinsRecombinant ProteinsRNA, CircularTET1 protein, humanTET1 protein, ratAstrocyteAutophagyCirc_0025984Ischemic strokemiR-143-3pORP150TET1

Identifiers

PMID34435328
OpenAlexW3193904034

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.