Evidence map›Paper›PMID 32139674›Full record

ArticleNature communications2020

Anti-angiogenic effects of VEGF stimulation on endothelium deficient in phosphoinositide recycling.

Amber N Stratman, Olivia M Farrelly, Constantinos M Mikelis, Mayumi F Miller, Zhiyong Wang, Van N Pham, Andrew E Davis, Margaret C Burns, Sofia A Pezoa, Daniel Castranova and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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  8. PI(4,5)PScience advances · 2023
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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

15 authors at 3 institutions in 4 countries.

Amber N StratmanDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0002-8111-4186
Olivia M Farrelly *Division of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Constantinos M Mikelis *Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, 20892, USA.
Mayumi F Miller *Division of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Zhiyong Wang *Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, 20892, USA.
Van N PhamDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Andrew E DavisDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Margaret C BurnsDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Sofia A PezoaDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Daniel CastranovaDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Joseph J YanoDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Tina M KiltsOral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, 20892, USA.
George E DavisDepartment of Molecular Pharmacology and Physiology, University of South Florida School of Medicine, Tampa, FL, 33612, USA.
J Silvio GutkindCraniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0002-5150-4482
Brant M WeinsteinDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA. flyingfish2@nih.gov.ORCID http://orcid.org/0000-0003-4136-4962
National Institutes of Health · USTexas Tech University · USUniversity of South Florida · US

Funding

Specification And Patterning of Developing Blood VesselsZIAHD001011 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI WEINSTEIN, BRANT · 2009 to 2025
$18.4M
Analysis of Mural Cell Ontogeny and Gene Function During Vascular DevelopmentR00HL125683 · NHLBI · WASHINGTON UNIVERSITY · PI STRATMAN, AMBER NICOLE · 2019 to 2021
$747k
NHLBI NIH HHS R00 HL125683
6 · The paper itself

Abstract

Anti-angiogenic therapies have generated significant interest for their potential to combat tumor growth. However, tumor overproduction of pro-angiogenic ligands can overcome these therapies, hampering success of this approach. To circumvent this problem, we target the resynthesis of phosphoinositides consumed during intracellular transduction of pro-angiogenic signals in endothelial cells (EC), thus harnessing the tumor's own production of excess stimulatory ligands to deplete adjacent ECs of the capacity to respond to these signals. Using zebrafish and human endothelial cells in vitro, we show ECs deficient in CDP-diacylglycerol synthase 2 are uniquely sensitive to increased vascular endothelial growth factor (VEGF) stimulation due to a reduced capacity to re-synthesize phosphoinositides, including phosphatidylinositol-(4,5)-bisphosphate (PIP2), resulting in VEGF-exacerbated defects in angiogenesis and angiogenic signaling. Using murine tumor allograft models, we show that systemic or EC specific suppression of phosphoinositide recycling results in reduced tumor growth and tumor angiogenesis. Our results suggest inhibition of phosphoinositide recycling provides a useful anti-angiogenic approach.

Indexed as

AllograftsAngiogenesis InhibitorsAnimalsCattleCell Line, TumorCell ProliferationDiacylglycerol CholinephosphotransferaseEndothelium, VascularGene DeletionHumansHuman Umbilical Vein Endothelial CellsMice, KnockoutModels, BiologicalNeovascularization, PhysiologicOrgan SpecificityPhosphatidylinositolsAngiogenesis InhibitorsDiacylglycerol CholinephosphotransferasePhosphatidylinositolsVascular Endothelial Growth Factors

Identifiers

PMID32139674
PMCPMC7058007
OpenAlexW3010486373

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.