Evidence map›Paper›PMID 33059750›Full record

ArticleStem cell research & therapy2020

TUG1 enhances high glucose-impaired endothelial progenitor cell function via miR-29c-3p/PDGF-BB/Wnt signaling.

Yang Li, Kangkang Zhi, Shilong Han, Xue Li, Maoquan Li, Weishuai Lian, Haijun Zhang, Xiaoping Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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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 2 institutions in 1 country.

Yang LiDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Kangkang ZhiDepartment of Vascular and Endovascular Surgery, Changzheng Hospital, Shanghai, 200003, China.
Shilong HanDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Xue LiDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Maoquan LiDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Weishuai LianDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China. lianweishuai@126.com.
Haijun ZhangDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China. ceo@brandentech.com.
Xiaoping ZhangDepartment of Interventional & Vascular Surgery, Tenth People's Hospital of Tongji University, Shanghai, 200072, China. zxpsibs@163.com.ORCID 0000-0002-1592-2353
Tongji University · CNShanghai Changzheng Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes is associated with the dysfunction of endothelial progenitor cells (EPCs), characterized as impaired angiogenesis, a phenomenon thought to be involved in the development of diabetic foot. lncRNA plays an essential role in microvascular dysfunction and signaling pathways in patients with diabetes. lncRNA taurine upregulated gene 1 (TUG1) participates in angiogenesis in various cells. However, the mechanisms of TUG1 activity in EPCs have not been elucidated.

methodsWe isolated and then characterized EPCs from the peripheral blood of mice using immunofluorescence and flow cytometry. Western blot detected the wnt/β-catenin pathway in high glucose-treated EPCs. Bioinformatics analysis predicted a putative binding site for TUG1 on miR-29c-3p. The interactions among TUG1, platelet-derived growth factor-BB (PDGF-BB), and miR-29c-3p were analyzed by luciferase assays. In vivo, diabetic mouse ischemic limb was treated with normal saline or TUG1 overexpression lentiviruses.

resultsWe found that EPC migration, invasion, and tube formation declined after treatment with high glucose, but improved with TUG1 overexpression. Mechanically, wnt/β-catenin pathway and autophagy were involved in the function of TUG1 overexpression in high glucose-treated EPCs. Moreover, TUG1 regulates the PDGF-BB/wnt pathway and function of high glucose-treated EPCs via miR-29c-3p. In vivo, injection of TUG1 lentivirus in a diabetic mouse ischemic limb model stimulated angiogenesis.

conclusionsOur findings suggest that TUG1 restores high glucose-treated EPC function by regulating miR-29c-3p/PDGF-BB/Wnt signaling.

Indexed as

BecaplerminEndothelial Progenitor CellsMicroRNAsRNA, Long NoncodingWnt Signaling PathwayAnimalsGlucoseMiceBecaplerminGlucoseMicroRNAsMIRN29 microRNA, mouseRNA, Long NoncodingTUG1 noncoding RNA, mouseAngiogenesisDiabetesEndothelial progenitor cellslncRNA taurine upregulated gene 1Platelet-derived growth factor-BB

Identifiers

PMID33059750
PMCPMC7558752
OpenAlexW3093414550

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Registered trials

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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.