Evidence map›Paper›PMID 38762650›Full record

ArticleScientific reports2024

miR-709 exerts an angiogenic effect through a FGF2 upregulation induced by a GSK3B downregulation.

Koji Ueno, Hiroshi Kurazumi, Ryo Suzuki, Masashi Yanagihara, Takahiro Mizoguchi, Takasuke Harada, Noriyasu Morikage, Kimikazu Hamano

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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.

Koji UenoDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan. kjueno@yamaguchi-u.ac.jp.ORCID 0000-0001-8629-0691
Hiroshi KurazumiDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Ryo SuzukiDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Masashi YanagiharaDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Takahiro MizoguchiDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Takasuke HaradaDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Noriyasu MorikageDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.
Kimikazu HamanoDepartment of Surgery and Clinical Science, Graduate School of Medicine, Yamaguchi University, Minami-Kogushi 1-1-1, Ube, Yamaguchi, 755-8505, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to identify angiogenic microRNAs (miRNAs) that could be used in the treatment of hindlimb ischemic tissues. miRNAs contained in extracellular vesicles (EVs) deriving from the plasma were analyzed in C57BL/6 mice, which have ischemia tolerance, and in BALB/c mice without ischemia tolerance as part of a hindlimb ischemia model; as a result 43 angiogenic miRNA candidates were identified. An aortic ring assay was employed by using femoral arteries isolated from BALC/c mice and EVs containing miRNA; as a result, the angiogenic miRNA candidates were limited to 14. The blood flow recovery was assessed after injecting EVs containing miRNA into BALB/c mice with hindlimb ischemia, and miR-709 was identified as a promising angiogenic miRNA. miR-709-encapsulating EVs were found to increase the expression levels of the fibroblast growth factor 2 (FGF2) mRNA in the thigh tissues of hindlimb ischemia model BALB/c mice. miR-709 was also found to bind to the 3'UTR of glycogen synthase kinase 3 beta (GSK3B) in three places. GSK3B-knockdown human artery-derived endothelial cells were found to express high levels of FGF2, and were characterized by increased cell proliferation. These findings indicate that miR-709 induces an upregulation of FGF2 through the downregulation of GSK3B.

Indexed as

Fibroblast Growth Factor 2Glycogen Synthase Kinase 3 betaHindlimbIschemiaMice, Inbred BALB CMicroRNAsNeovascularization, Physiologic3' Untranslated RegionsAnimalsCell ProliferationDisease Models, AnimalDown-RegulationEndothelial CellsExtracellular VesiclesHumansMale3' Untranslated RegionsFibroblast Growth Factor 2Glycogen Synthase Kinase 3 betaGsk3b protein, mouseMicroRNAsAngiogenesisExtracellular vesiclesFGF2GSK3BmiR-709miRNA

Identifiers

PMID38762650
PMCPMC11102560

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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.