Evidence map›Paper›PMID 31709761›Full record

ArticleJournal of cellular and molecular medicine2020

Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir-145 to up-regulate AQP4 expression.

Weifeng Shan, Wei Chen, Xian Zhao, Aijie Pei, Manli Chen, Yang Yu, Yueying Zheng, Shengmei Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.1field-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

41 citing papers in PubMed, 54 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

8 authors at 2 institutions in 1 country.

Weifeng ShanDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Wei ChenCancer Institute of Integrated traditional Chinese and Western Medicine, Zhejiang Academy of Traditional Chinese Medicine, Tongde hospital of Zhejiang Province, Hangzhou, China.ORCID 0000-0002-0399-6216
Xian ZhaoDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Aijie PeiDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Manli ChenDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Yang YuDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Yueying ZhengDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Shengmei ZhuDepartment of Anesthesiology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.ORCID 0000-0001-9763-4015
Second Affiliated Hospital of Zhejiang University · CNTongde Hospital of Zhejiang Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging studies have shown that long noncoding RNA (lncRNA) TUG1 (taurine-up-regulated gene 1) plays critical roles in multiple biological processes. However, the expression and function of lncRNA TUG1 in cerebral ischaemia/reperfusion injury have not been reported yet. In this study, we found that LncRNA TUG1 expression was significantly up-regulated in cultured MA-C cells exposed to OGD/R injury, while similar results were also observed in MCAO model. Mechanistically, knockdown of TUG1 decreased lactate dehydrogenase levels and the ratio of apoptotic cells and promoted cell survival in vitro. Moreover, knockdown of TUG1 decreased AQP4 (encoding aquaporin 4) expression to attenuate OGD/R injury. TUG1 could interact directly with miR-145, and down-regulation of miR-145 could efficiently reverse the function of TUG1 siRNA on AQP4 expression. Finally, the TUG1 shRNA reduced the infarction area and cell apoptosis in I/R mouse brains in vivo. In summary, our results suggested that lncRNA TUG1 may function as a competing endogenous RNA (ceRNA) for miR-145 to induce cell damage, possibly providing a new therapeutic target in cerebral ischaemia/reperfusion injury.

Indexed as

AnimalsApoptosisAquaporin 4Base SequenceBrain IschemiaGene Knockdown TechniquesGlucoseMaleMice, Inbred C57BLMicroRNAsOxygenReperfusion InjuryRNA, Long NoncodingRNA, Small InterferingUp-RegulationAquaporin 4Glucoselong non-coding RNA TUG1, mouseMicroRNAsMIRN145a microRNA, mouseOxygenRNA, Long NoncodingRNA, Small InterferingAquaporin-4cerebral ischaemialncTUG1miR-145reperfusion injury

Identifiers

PMID31709761
PMCPMC6933375
OpenAlexW2983577881

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.