Evidence map›Paper›PMID 28097093›Full record

ArticleFEBS open bio2017

Vascular endothelial growth factor suppresses TNFSF15 production in endothelial cells by stimulating miR-31 and miR-20a expression via activation of Akt and Erk signals.

Hui-Ting Deng, Hai-Lin Liu, Bei-Bei Zhai, Kun Zhang, Guo-Ce Xu, Xue-Mei Peng, Qiang-Zhe Zhang, Lu-Yuan Li

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  15. The regulatory role of microRNAs in angiogenesis-related diseases.Journal of cellular and molecular medicine · 2018
    Review
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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 3 institutions in 1 country.

Hui-Ting DengState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Hai-Lin LiuState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Bei-Bei ZhaiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Kun ZhangState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Guo-Ce XuState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Xue-Mei PengState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Qiang-Zhe ZhangState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Lu-Yuan LiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research Nankai University China; Collaborative Innovation Center for Biotherapy Nankai University West China Hospital Sichuan University Chengdu China.
Sichuan University · CNState Key Laboratory of Medicinal Chemical BiologyNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor superfamily-15 (TNFSF15; VEGI; TL1A) is a negative modulator of angiogenesis for blood vessel homeostasis and is produced by endothelial cells in a mature vasculature. It is known to be downregulated by vascular endothelial growth factor (VEGF), a major regulator of neovascularization but the mechanism of this interaction is unclear. Here we report that VEGF is able to stimulate the production of two microRNAs, miR-20a and miR-31, which directly target the 3'-UTR of TNFSF15. Additionally, we show that two VEGF-stimulated cell growth signals, Erk and Akt, are responsible for promoting the expression of miR-20a and miR-31. Treatment of human umbilical vein endothelial cells (HUVECs) with Akt inhibitor LY294002 results in diminished miR-20a and miR-31 production, while Erk inhibitor U0126 prevented VEGF-stimulated expression of miR-20a but not that of miR-31. Furthermore, inactivation of either Erk or Akt signals restores TNFSF15 gene expression. In an angiogenesis assay, elevated miR-20a or miR-31 levels in HUVECs leads to enhancement of capillary-like tubule formation

Indexed as

AktErkmiRNATNFSF15VEGF

Identifiers

PMID28097093
PMCPMC5221472
OpenAlexW2560061338

What OpenQuestion holds

Textmetadata
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.