Evidence map›Paper›PMID 28849133›Full record

ArticleMolecular medicine reports2017

Downregulation of microRNA-195 promotes angiogenesis induced by cerebral infarction via targeting VEGFA.

Wen-Jing Zhao, Hai-Fang Zhang, Jin-Ying Su

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Angiogenesis after ischemic stroke.Acta pharmacologica Sinica · 2023
    Review
  3. Article
  4. Review
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  15. Article
  16. MicroRNAs in brain development and cerebrovascular pathophysiology.American journal of physiology. Cell physiology · 2019
    Review
  17. Article
  18. Article
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Wen-Jing ZhaoDepartment of Neurology, The Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056002, P.R. China.
Hai-Fang ZhangHandan Emergency Rescue Command Center, Handan, Hebei 056002, P.R. China.
Jin-Ying SuDepartment of Neurology, The Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056002, P.R. China.
Affiliated Hospital of Hebei University · CNHandan College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis, the formation of new blood vessels from preexisting endothelium, is a process that involves a series of interassociated and mutually interactive pathophysiological processes. It is accepted that microRNAs (miRNAs) regulate endothelial cell behavior, including their involvement in angiogenesis. However, it remains unclear whether miRNAs are involved in the regulation of angiogenesis following cerebral ischemia. Therefore, the present study aimed to investigate the role of miRNAs in angiogenesis and the underlying mechanism following cerebral ischemia. Expression profiles of miRNAs in rat brain samples following middle cerebral artery occlusion (MCAO) were investigated using a miRNA microarray. The expression of candidate miRNA, miR‑195 was further validated using reverse transcription‑quantitative polymerase chain reaction. Then, the effects of miR‑195 on cell migration and tube formation of human umbilical vein vascular endothelial cells (HUVECs) were investigated following miR‑195 silencing, and overexpression. The specific target genes of miR‑195 were predicted using microRNA prediction bioinformatics software (http://www.microrna.org/microrna/home.do), and then confirmed using a dual‑luciferase reporter assay and rescue experiment. It was demonstrated that miR‑195 was significantly downregulated in the brains of rats following MCAO and in hypoxia‑induced HUVECs. Furthermore, it was revealed that miR‑195 overexpression inhibited the invasion ability and tube formation of HUVECs in vitro, while miR‑195 silencing enhanced these functions. In addition, vascular endothelial growth factor A (VEGFA) was identified as a direct target of miR‑195 and was negatively correlated with miR‑195 expression. In addition, the rescue experiment revealed that overexpression of VEGFA reversed the inhibitory effects of miR‑195 overexpression on the invasion ability and tube formation of HUVECs. The present study has provided a novel insight into the promoting roles of miR‑195 downregulation on angiogenesis following cerebral infarction and suggests that the miR‑195/VEGFA signaling pathway is a putative therapeutic target in cerebral ischemia.

Indexed as

Gene Expression RegulationRNA InterferenceAnimalsCell MovementCerebral InfarctionCluster AnalysisGene Expression ProfilingHumansHuman Umbilical Vein Endothelial CellsMaleMicroRNAsNeovascularization, PhysiologicRatsVascular Endothelial Growth Factor AMicroRNAsMIRN195 microRNA, ratVascular Endothelial Growth Factor A

Identifiers

PMID28849133
PMCPMC5647088
OpenAlexW2742236243

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.