Evidence map›Paper›PMID 25966978›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2015

Adenosine A2B receptor stimulates angiogenesis by inducing VEGF and eNOS in human microvascular endothelial cells.

Xiaolong Du, Xuehai Ou, Tao Song, Wentao Zhang, Fei Cong, Shihui Zhang, Yongmin Xiong

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 72 citations in OpenAlex.

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  9. Blockage of the adenosine APurinergic signalling · 2024
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  12. Ivy Leaf Dry Extract EA 575International journal of molecular sciences · 2023
    Article
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  16. An overview of current therapeutic strategies for glioblastoma and the role of CD73 as an alternative curative approach.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    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

7 authors at 2 institutions in 1 country.

Xiaolong DuInstitute of Endemic Diseases, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an Jiaotong University, Xi'an Shaanxi 710061, China.
Xuehai OuSchool of Medicine, Xi'an Jiao Tong University, Xi'an Shaanxi 710061, China.
Tao SongSchool of Medicine, Xi'an Jiao Tong University, Xi'an Shaanxi 710061, China.
Wentao ZhangSchool of Medicine, Xi'an Jiao Tong University, Xi'an Shaanxi 710061, China.
Fei CongSchool of Medicine, Xi'an Jiao Tong University, Xi'an Shaanxi 710061, China.
Shihui ZhangSchool of Medicine, Xi'an Jiao Tong University, Xi'an Shaanxi 710061, China.
Yongmin XiongInstitute of Endemic Diseases, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an Jiaotong University, Xi'an Shaanxi 710061, China xiongyongmin@126.com.
Xi'an Jiaotong University · CNNational Health and Family Planning Commission · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is critical to wound repair due to its role in providing oxygen and nutrients that are required to support the growth and function of reparative cells in damaged tissues. Adenosine receptors are claimed to be of paramount importance in driving wound angiogenesis by inducing VEGF. However, the underlying mechanisms for the regulation of adenosine receptors in VEGF as well as eNOS remain poorly understood. In the present study, we found that adenosine and the non-selective adenosine receptor agonists (NECA) induced tube formation in HMEC-1 in a dose-dependent manner. Adenosine or NECA (10 µmol/L) significantly augmented the number and length of the segments in comparison with the control. Simultaneously, VEGF and eNOS were significantly upregulated following the administration of 10 µmol/L NECA, while they were suppressed after A2B AR genetic silencing and pharmacological inhibition by MRS1754. In addition, VEGF expression and eNOS bioavailability elimination significantly reduced the formation of capillary-like structures. Furthermore, the activation of A2B AR by NECA significantly increased the intracellular cAMP levels and concomitant CREB phosphorylation, eventually leading to the production of VEGF in HMEC-1. However, the activated PKA-CREB pathway seemed to be invalidated in the induction of eNOS. Moreover, we found that the elicited PI3K/AKT signaling in response to the induction of NECA assisted in regulating eNOS but failed to impact on VEGF generation. In conclusion, the A2B AR activation-driven angiogenesis via cAMP-PKA-CREB mediated VEGF production and PI3K/AKT-dependent upregulation of eNOS in HMEC-1.

Indexed as

Neovascularization, PhysiologicAcetamidesAdenosineCapillariesCell LineCyclic AMPDose-Response Relationship, DrugEndothelial CellsGene Expression Regulation, EnzymologicHumansMicrocirculationNitric Oxide Synthase Type IIIOxygenPhosphatidylinositol 3-KinasesPhosphorylationPurinesAcetamidesAdenosineCyclic AMPN-(4-cyanophenyl)-2-(4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)-phenoxy)acetamideNitric Oxide Synthase Type IIINOS3 protein, humanOxygenPhosphatidylinositol 3-KinasesPurinesReceptor, Adenosine A2BRNA, Small InterferingVascular Endothelial Growth Factor AVEGFA protein, humanAdenosine A2B receptorangiogenesisCREBeNOSVEGF

Identifiers

PMID25966978
PMCPMC4935298
OpenAlexW1783256508

What OpenQuestion holds

Textmetadata
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.