Evidence map›Paper›PMID 34146216›Full record

ArticleMetabolic brain disease2021

Circ_0006768 upregulation attenuates oxygen-glucose deprivation/reoxygenation-induced human brain microvascular endothelial cell injuries by upregulating VEZF1 via miR-222-3p inhibition.

Jing Li, Jiguang Wang, Zhi Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  9. The Role of Circular RNAs in Ischemic Stroke.Neurochemical research · 2023
    Review
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  11. Article
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  14. Article
  15. Article
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  18. Review
  19. The regulatory roles of circular RNAsFrontiers in neurology · 2022
    Review
  20. Review
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

3 authors at 1 institution in 1 country.

Jing LiDepartment of Internal Medicine-Neurology, Hengshui People's Hospital, No. 180, Renmin East Road, Hengshui, 053000, China.
Jiguang WangDepartment of Internal Medicine-Neurology, Hengshui People's Hospital, No. 180, Renmin East Road, Hengshui, 053000, China. wangjiguang0901@126.com.
Zhi WangDepartment of Internal Medicine-Neurology, Hengshui People's Hospital, No. 180, Renmin East Road, Hengshui, 053000, China.
Hengshui University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular RNAs (circRNAs) have been widely implicated in multiple diseases, including ischemic stroke. This study aimed to explore the function and functional mechanism of circ_0006768 in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced brain injury models of ischemic stroke. Human brain microvascular endothelial cells (HBMECs) were induced by OGD/R to mimic ischemic stroke models in vitro. The expression of circ_0006768, microRNA-222-3p (miR-222-3p) and vascular endothelial zinc finger 1 (VEZF1) was detected by quantitative real-time PCR (qPCR). Cell viability, angiogenesis ability and cell migration were assessed by cell counting kit-8 (CCK-8) assay, tube formation assay and wound healing assay, respectively. The releases of pro-inflammatory factors were determined by commercial enzyme-linked immunosorbent assay (ELISA) kits. The protein levels of vascular endothelial growth factor A (VEGFA), N-cadherin and VEZF1 were detected by western blot. The putative relationship between miR-222-3p and circ_0006768 or VEZF1 was validated by dual-luciferase reporter assay, RNA Immunoprecipitation (RIP) assay and pull-down assay. Circ_0006768 was poorly expressed in ischemic stroke plasma and OGD/R-induced HBMECs. OGD/R inhibited cell viability, angiogenesis and cell migration and promoted the releases of pro-inflammatory factors, while circ_0006768 overexpression or miR-222-3p inhibition partially abolished the effects of OGD/R. MiR-222-3p was targeted by circ_0006768, and VEZF1 was a target of miR-222-3p. Circ_0006768 enriched the expression of VEZF1 via mediating miR-222-3p inhibition. Rescue experiments presented that the effects of circ_0006768 overexpression were reversed by miR-222-3p restoration or VEZF1 knockdown. Circ_0006768 overexpression attenuates OGD/R-induced HBMEC injuries by upregulating VEZF1 via miR-222-3p inhibition.

Indexed as

Brain InjuriesMicroRNAsBrainDNA-Binding ProteinsEndothelial CellsGlucoseHumansOxygenTranscription FactorsUp-RegulationVascular Endothelial Growth Factor ADNA-Binding ProteinsGlucoseMicroRNAsMIR222, humanOxygenTranscription FactorsVascular Endothelial Growth Factor AVEZF1 protein, humancirc_0006768Ischemic strokemiR-222-3pOGD/RVEZF1

Identifiers

PMID34146216
OpenAlexW3172953938

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.