Evidence map›Paper›PMID 30950039›Full record

ArticleJournal of cellular physiology2019

Activation of the STAT3/microRNA-21 pathway participates in angiotensin II-induced angiogenesis.

Li-Yuan Chen, Xue Wang, Xiao-Long Qu, Li-Na Pan, Ze-Yang Wang, Yong-Hui Lu, Hou-Yuan Hu

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

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  20. STAT3 Regulates miR-384 Transcription During Th17 Polarization.Frontiers in cell and developmental biology · 2019
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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

7 authors at 1 institution in 1 country.

Li-Yuan ChenDepartment of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xue WangDepartment of Occupational Health, Third Military Medical University, Chongqing, China.
Xiao-Long QuDepartment of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Li-Na PanDepartment of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Ze-Yang WangDepartment of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Yong-Hui LuDepartment of Occupational Health, Third Military Medical University, Chongqing, China.
Hou-Yuan HuDepartment of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.ORCID 0000-0003-2237-2115
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (AngII) facilitates angiogenesis that is associated with the continuous progression of atherosclerotic plaques, but the underlying mechanisms are still not fully understood. Several microRNAs (miRNAs) have been shown to promote angiogenesis; however, whether miRNAs play a crucial role in AngII-induced angiogenesis remains unclear. This study evaluated the functional involvement of miRNA-21 (miR-21) in the AngII-mediated proangiogenic response in human microvascular endothelial cells (HMECs). We found that AngII exerted a proangiogenic role, indicated by the promotion of proliferation, migration, and tube formation in HMECs. Next, miR-21 was found to be upregulated in AngII-treated HMECs, and its specific inhibitor potently blocked the proangiogenic effects of AngII. Subsequently, we focused on the constitutive activation of STAT3 in the AngII-mediated proangiogenic process. Bioinformatic analysis indicated that STAT3 acted as a transcription factor initiating miR-21 expression, which was verified by ChIP-PCR. A reporter assay further identified three functional binding sites of STAT3 in the miR-21 promoter region. Moreover, phosphatase and tensin homolog (PTEN) was recognized as a target of miR-21, and STAT3 inhibition restored AngII-induced reduction in PTEN. Similarly, the STAT3/miR-21 axis was shown to mediate AngII-provoked angiogenesis in vivo, which was demonstrated by using the appropriate inhibitors. Our data suggest that AngII was involved in proangiogenic responses through miR-21 upregulation and reduced PTEN expression, which was, at least in part, linked to STAT3 signaling. The present study provides novel insights into AngII-induced angiogenesis and suggests potential treatment strategies for attenuating the progression of atherosclerotic lesions and preventing atherosclerosis complications.

Indexed as

Angiogenesis Inducing AgentsAngiotensin IIAnimalsCell MovementCell ProliferationEndothelial CellsGene Expression RegulationHumansMiceMicroRNAsNeovascularization, PathologicPlaque, AtheroscleroticPTEN PhosphohydrolaseSignal TransductionSTAT3 Transcription FactorAngiogenesis Inducing AgentsAngiotensin IIMicroRNAsMIRN21 microRNA, humanPTEN PhosphohydrolaseSTAT3 Transcription Factorangiogenesisangiotensin IIatherosclerosismiR-21STAT3

Identifiers

PMID30950039
PMCPMC6767590
OpenAlexW2929574748

What Socratic 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 Socratic graph.