Evidence map›Paper›PMID 26857067›Full record

ArticleJournal of the American Heart Association2016

miR-342-5p Is a Notch Downstream Molecule and Regulates Multiple Angiogenic Pathways Including Notch, Vascular Endothelial Growth Factor and Transforming Growth Factor β Signaling.

Xian-Chun Yan, Jing Cao, Liang Liang, Li Wang, Fang Gao, Zi-Yan Yang, Juan-Li Duan, Tian-Fang Chang, San-Ming Deng, Yuan Liu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-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

36 citing papers in PubMed, 65 citations in OpenAlex.

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  11. N6-Adenosine Methylation (mJournal of cardiovascular translational research · 2021
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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

15 authors at 2 institutions in 1 country.

Xian-Chun YanState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jing CaoState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China Department of Respiratory Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Liang LiangState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Li WangState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Fang GaoState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Zi-Yan YangState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Juan-Li DuanState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Tian-Fang ChangState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China Department of Ophthalmology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
San-Ming DengState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Yuan LiuState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Guo-Rui DouDepartment of Ophthalmology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jian ZhangDepartment of Respiratory Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Qi-Jun ZhengDepartment of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Ping ZhangState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hua HanState Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Xijing Hospital, Fourth Military Medical University, Xi'an, China huahan@fmmu.edu.cn.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial cells (ECs) form blood vessels through angiogenesis that is regulated by coordination of vascular endothelial growth factor (VEGF), Notch, transforming growth factor β, and other signals, but the detailed molecular mechanisms remain unclear. METHODS AND

resultsSmall RNA sequencing initially identified miR-342-5p as a novel downstream molecule of Notch signaling in ECs. Reporter assay, quantitative reverse transcription polymerase chain reaction and Western blot analysis indicated that miR-342-5p targeted endoglin and modulated transforming growth factor β signaling by repressing SMAD1/5 phosphorylation in ECs. Transfection of miR-342-5p inhibited EC proliferation and lumen formation and reduced angiogenesis in vitro and in vivo, as assayed by using a fibrin beads-based sprouting assay, mouse aortic ring culture, and intravitreal injection of miR-342-5p agomir in P3 pups. Moreover, miR-342-5p promoted the migration of ECs, accompanied by reduced endothelial markers and increased mesenchymal markers, indicative of increased endothelial-mesenchymal transition. Transfection of endoglin at least partially reversed endothelial-mesenchymal transition induced by miR-342-5p. The expression of miR-342-5p was upregulated by transforming growth factor β, and inhibition of miR-342-5p attenuated the inhibitory effects of transforming growth factor β on lumen formation and sprouting by ECs. In addition, VEGF repressed miR-342-5p expression, and transfection of miR-342-5p repressed VEGFR2 and VEGFR3 expression and VEGF-triggered Akt phosphorylation in ECs. miR-342-5p repressed angiogenesis in a laser-induced choroidal neovascularization model in mice, highlighting its clinical potential.

conclusionsmiR-342-5p acts as a multifunctional angiogenic repressor mediating the effects and interaction among angiogenic pathways.

Indexed as

3' Untranslated RegionsAnimalsBinding SitesCell Adhesion MoleculesCell MovementCell ProliferationChoroidal NeovascularizationDisease Models, AnimalEndoglinEpithelial-Mesenchymal TransitionHeLa CellsHumansHuman Umbilical Vein Endothelial CellsMice, Inbred BALB CMice, TransgenicMicroRNAs3' Untranslated RegionsCell Adhesion MoleculesEndoglinENG protein, humanEVL protein, humanMicroRNAsMIRN342 microRNA, humanMirn342 microRNA, mouseNOTCH1 protein, humanNotch1 protein, mouseProto-Oncogene Proteins c-aktReceptor, Notch1Transforming Growth Factor betaVascular Endothelial Growth Factor Aangiogenesisendothelial cellendothelial cell differentiationmicroRNANotchvascular endothelial growth factor

Identifiers

PMID26857067
PMCPMC4802463
OpenAlexW2267105610

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.