Evidence map›Paper›PMID 34709972›Full record

ArticleBioengineered2021

Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG.

Xinyu Zhou, Zhonglong Wang, Bingchao Xu, Niu Ji, Pin Meng, Lei Gu, Ying Li

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioengineered, 2021. 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
2.7field-weighted citation impact, top 8% 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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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 3 institutions in 1 country.

Xinyu ZhouDepartment of Neurology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, the First People's Hospital of Lianyungang, Lianyungang, Jiangsu Province, China.
Zhonglong WangDepartment of Neurology, Jining Psychiatric Hospital, Jining, Shandong Province, China.
Bingchao XuDepartment of Neurology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, the First People's Hospital of Lianyungang, Lianyungang, Jiangsu Province, China.
Niu JiDepartment of Neurology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, the First People's Hospital of Lianyungang, Lianyungang, Jiangsu Province, China.
Pin MengDepartment of Neurology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, the First People's Hospital of Lianyungang, Lianyungang, Jiangsu Province, China.
Lei GuRehabilitation Center, Beijing Xiaotangshan Hospital, Beijing, China.
Ying LiRehabilitation Center, Beijing Xiaotangshan Hospital, Beijing, China.
The First People’s Hospital of Lianyungang · CNTang Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LncRNAs are identified as critical regulators in cerebral ischemia/reperfusion injury (CIRI). In this current work, SH-SY5Y cells suffered from oxygen-glucose deprivation/reperfusion (OGD/R) were applied to analyze the biological role of lncRNA NORAD and underlying molecular mechanism in CIRI in vitro. Levels of lncRNA NORAD, miR-30a-5p and YWHAG were measured using RT-qPCR. Bioinformatics analysis predicted the binding sites of lncRNA NORAD to miR-30a-5p and miR-30a-5p to YWHAG. Luciferase reporter assay verified the binding relationships among lncRNA NORAD, miR-30a-5p and YWHAG. Additionally, cell viability was determined using CCK-8 assay, and cell apoptosis was assessed using TUNEL staining and western blot analysis. Moreover, the levels of ROS, MDA, LDH and SOD as well as IL-1β, TNF-α, and IL-6 were assessed via application of the corresponding assay kits. Decreased cell viability and temporarily increased lncRNA NORAD level were observed in SH-SY5Y cells after OGD/R. It was demonstrated that lncRNA NORAD regulated YWHAG expression by sponging miR-30a-5p. Upregulation of lncRNA NORAD contributed to the enhancement of cell viability, the inhibition of cell apoptosis as well as the alleviation of oxidative stress and inflammation in OGD/R-injured SH-SY5Y cells, which were reversed upon elevation of miR-30a-5p. In contrast, downregulation of lncRNA NORAD reduced cell viability, promoted cell apoptosis as well as aggravated oxidative stress and inflammation under OGD/R challenge, and the functions of lncRNA NORAD knockdown in OGD/R injury were abolished by upregulation of YWHAG. Taken together, lncRNA NORAD exerted protective effects against OGD/R-induced neural injury by sponging miR-30a-5p to upregulate YWHAG expression.

Indexed as

14-3-3 ProteinsApoptosisBase SequenceBrainBrain IschemiaCell Line, TumorCell SurvivalGene Expression RegulationGlucoseHumansInflammationMicroRNAsOxidative StressOxygenReperfusion InjuryRNA, Long Noncoding14-3-3 ProteinsGlucoseMicroRNAsMIRN30a microRNA, humanNORAD long non-coding RNA, humanOxygenRNA, Long NoncodingYWHAG protein, humancerebral ischemia/reperfusion injuryLncRNA NORADmiR-30a-5pOGD/R injuryYWHAG

Identifiers

PMID34709972
PMCPMC8810080
OpenAlexW3209000550

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.