Evidence map›Paper›PMID 28114883›Full record

ArticleBMC cell biology2017

Release of endothelial cell associated VEGFR2 during TGF-β modulated angiogenesis in vitro.

M Jarad, E A Kuczynski, J Morrison, A M Viloria-Petit, B L Coomber

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

Article in BMC cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-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

33 citing papers in PubMed, 62 citations in OpenAlex.

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  9. Scalable Generation of Pre-Vascularized and Functional Human Beige Adipose Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  10. Article
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  12. Exosomes as Novel Diagnostic Biomarkers and Therapeutic Tools in Gliomas.International journal of molecular sciences · 2023
    Review
  13. Activin A Limits VEGF-Induced Permeability via VE-PTP.International journal of molecular sciences · 2023
    Article
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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

5 authors at 1 institution in 1 country.

M JaradDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, OVC Room 3645, Guelph, N1G 2W1, ON, Canada.
E A KuczynskiDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, OVC Room 3645, Guelph, N1G 2W1, ON, Canada.
J MorrisonDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, OVC Room 3645, Guelph, N1G 2W1, ON, Canada.
A M Viloria-PetitDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, OVC Room 3645, Guelph, N1G 2W1, ON, Canada.
B L CoomberDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, OVC Room 3645, Guelph, N1G 2W1, ON, Canada. bcoomber@uoguelph.ca.
University of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSprouting angiogenesis requires vascular endothelial proliferation, migration and morphogenesis. The process is regulated by soluble factors, principally vascular endothelial growth factor (VEGF), and via bidirectional signaling through the Jagged/Notch system, leading to assignment of tip cell and stalk cell identity. The cytokine transforming growth factor beta (TGF-β) can either stimulate or inhibit angiogenesis via its differential surface receptor signaling. Here we evaluate changes in expression of angiogenic signaling receptors when bovine aortic endothelial cells were exposed to TGF-β1 under low serum conditions.

resultsTGF-β1 induced a dose dependent inhibition of tip cell assignment and subsequent angiogenesis on Matrigel, maximal at 5.0 ng/ml. This occurred via ALK5-dependent pathways and was accompanied by significant upregulation of the TGF-β co-receptor endoglin, and SMAD2 phosphorylation, but no alteration in Smad1/5 activation. TGF-β1 also induced ALK5-dependent downregulation of Notch1 but not of its ligand delta-like ligand 4. Cell associated VEGFR2 (but not VEGFR1) was significantly downregulated and accompanied by reciprocal upregulation of VEGFR2 in conditioned medium. Quantitative polymerase chain reaction analysis revealed that this soluble VEGFR2 was not generated by a selective shift in mRNA isoform transcription. This VEGFR2 in conditioned medium was full-length protein and was associated with increased soluble HSP-90, consistent with a possible shedding of microvesicles/exosomes.

conclusionsTaken together, our results suggest that endothelial cells exposed to TGF-β1 lose both tip and stalk cell identity, possibly mediated by loss of VEGFR2 signaling. The role of these events in physiological and pathological angiogenesis requires further investigation.

Indexed as

Neovascularization, PhysiologicAnimalsCattleEndothelial CellsHumansProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta1Vascular Endothelial Growth Factor Receptor-2Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanTransforming Growth Factor betaTransforming Growth Factor beta1Vascular Endothelial Growth Factor Receptor-2Dll4MicroparticleNotch1Smad signalingTip cellVascular sprouting

Identifiers

PMID28114883
PMCPMC5260130
OpenAlexW2582495616

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.