Evidence map›Paper›PMID 39017855›Full record

ArticleJournal of molecular histology2024

TUG1 exacerbates cerebral ischemia-reperfusion injury through miR-340-5p-mediated PTEN.

Fei Li, Hui-Kai Zhang, Hong-Xiang Jiang, Xin-Yuan Zhang, Qian-Xue Chen

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Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Article
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4 · The record

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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.

Fei LiDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Hui-Kai ZhangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Hong-Xiang JiangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Xin-Yuan ZhangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Qian-Xue ChenDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China. chenqx666@sohu.com.

Funding

National Natural Science Foundation of China 82071299
6 · The paper itself

Abstract

Long non-coding RNAs (LncRNAs) play a substantial role in the process of cerebral ischemia-reperfusion injury (CIRI). The present work aimed to determine the probable mechanism by which LncRNA TUG1 exacerbates CIRI via the miR-340-5p/phosphatase and tensin homolog (PTEN) pathway. After developing a middle cerebral artery occlusion/reperfusion (MCAO/R) model, pcDNA-TUG1 together with miR-340-5p agomir were administrated in vivo. Furthermore, the neurologic defects in rats were assessed by a modified neurological severity score. Moreover, 2,3,5-Triphenyl-2 H-tetrazolium chloride stain-step was performed to determine the brain's infarct size. In addition, western blotting, immunohistochemistry, and qRT-PCR experiments were utilized for gauging the proteomic/genomic expression-profiles. Luciferase reporter assay validated correlations across TUG1, miR-340-5p, together with PTEN. The results indicated relatively reduced miR-340-5p levels in MCAO/R models, while upregulated TUG1 levels. The pcDNA-TUG1-treated rats indicated increasing neurological dysfunction, whereas the miR-340-5p agomir-treated rats showed improvement. Furthermore, miR-340-5p was determined to be the expected and confirmed TUG1 target. All things considered, the findings suggested that PTEN can serve as the target of miR-340-5p. In addition, TUG1 served as a miR-340-5p ceRNA, which promotes PTEN modulation. Furthermore, TUG1 overexpression decreased miR-340-5p's capacity to fend against CIRI. Conclusively, this work proved that in CIRI, targeting the TUG1/miR-340-5p/PTEN regulatory axis is a viable approach for the treatment of ischemic stroke.

Indexed as

MicroRNAsPTEN PhosphohydrolaseReperfusion InjuryRNA, Long NoncodingAnimalsBrain IschemiaDisease Models, AnimalGene Expression RegulationInfarction, Middle Cerebral ArteryMaleRatsRats, Sprague-DawleyMicroRNAsMIRN340-1 microRNA, ratPTEN PhosphohydrolasePten protein, ratRNA, Long NoncodingTUG1 long noncoding RNA, ratCerebral ischemia-reperfusion injuryIschemic strokemiR-340-5pPhosphatase and tensin homologTaurine-upregulated gene 1

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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.