Evidence map›Paper›PMID 32332879›Full record

ArticleScientific reports2020

Circ-camk4 involved in cerebral ischemia/reperfusion induced neuronal injury.

Zhao-Huan Zhang, Yue-Rong Wang, Fei Li, Xiu-Ling Liu, Hui Zhang, Zhong-Zheng Zhu, Hai Huang, Xiao-Hui Xu

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

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 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 4 institutions in 1 country.

Zhao-Huan Zhang *School of Preclinical Medicine, Wannan Medical College, Wuhu 241001, China. School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Yue-Rong Wang *School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Fei Li *Department of Neurology, Changzheng Hospital, 200003, Shanghai, China.
Xiu-Ling LiuSchool of Life Sciences, Shanghai University, Shanghai, 200444, China.
Hui ZhangSchool of Life Sciences, Shanghai University, Shanghai, 200444, China.
Zhong-Zheng ZhuDepartment of Oncology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Hai HuangSchool of Life Sciences, Shanghai University, Shanghai, 200444, China.
Xiao-Hui XuSchool of Preclinical Medicine, Wannan Medical College, Wuhu 241001, China. School of Life Sciences, Shanghai University, Shanghai, 200444, China. xxhxxh@shu.edu.cn.ORCID http://orcid.org/0000-0001-7608-4114
Shanghai University · CNWannan Medical College · CNShanghai Changzheng Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke and subsequent cerebral ischemia/reperfusion (I/R) injury is a frequently occurring disease that can have serious consequences in the absence of timely intervention. Circular RNAs (circRNAs) in association with microRNAs (miRNAs) and RNA-binding proteins (RBPs) can influence gene expression. However, whether circRNAs have a role in cerebral I/R injury pathogenesis, especially soon after onset, is unclear. In this study, we used the SD rat middle cerebral artery occlusion (MCAO) model of stroke to examine the role of circRNAs in cerebral I/R injury. We used high-throughput sequencing (HTS) to compare the expression levels of circRNAs in cerebral cortex tissue from MCAO rats during the occlusion-reperfusion latency period 3 hours after I/R injury with those in control cerebral cortices. Our sequencing results revealed that expression levels of 44 circRNAs were significantly altered after I/R, with 16 and 28 circRNAs showing significant up- and down-regulation, respectively, relative to levels in control cortex. We extended these results in vitro in primary cultured neuron cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R) using qRT-PCR to show that levels of circ-camk4 were increased in OGD/R neurons relative to control neurons. Bioinformatics analyses predicted that several miRNAs could be associated with circ-camk4 and this prediction was confirmed in a RNA pull-down assay. KEGG analysis to predict pathways that involve circ-camk4 included the glutamatergic synapse pathway, MAPK signaling pathway, and apoptosis signaling pathways, all of which are known to be involved in brain injury after I/R. Our results also demonstrate that levels of the human homolog to circ-camk4 (hsa-circ-camk4) are elevated in SH-SY5Y cells exposed to OGD/R treatment. Overexpression of hsa-circ-camk4 in SH-SY5Y cells significantly increased the rate of cell death after OGD/R, suggesting that circ-camk4 may play a key role in progression of cerebral I/R injury.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 4Cell LineCerebral Arterial DiseasesComputational BiologyHumansMaleNervous System DiseasesRatsRats, Sprague-DawleyReperfusion InjuryRNA, CircularStrokeCalcium-Calmodulin-Dependent Protein Kinase Type 4Camk4 protein, ratRNA, Circular

Identifiers

PMID32332879
PMCPMC7181679
OpenAlexW3018825385

What OpenQuestion holds

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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.