Evidence map›Paper›PMID 24022223›Full record

ArticlePhysiological genomics2013

Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress.

Brian R Hoffmann, Jordan R Wagner, Anthony R Prisco, Agnieszka Janiak, Andrew S Greene

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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, 31 citations in OpenAlex.

  1. Article
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  8. Article
  9. lncRNA HOTAIR Protects Myocardial Infarction Rat by Sponging miR-519d-3p.Journal of cardiovascular translational research · 2019
    Article
  10. Article
  11. Article
  12. Emerging role of dopamine in neovascularization of pheochromocytoma and paraganglioma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Review
  13. Article
  14. Mechanisms of Mas1 Receptor-Mediated Signaling in the Vascular Endothelium.Arteriosclerosis, thrombosis, and vascular biology · 2017
    Article
  15. Review
  16. Review
  17. 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.

Brian R HoffmannBiotechnology and Bioengineering Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and.
Jordan R Wagner
Anthony R Prisco
Agnieszka Janiak
Andrew S Greene
Medical College of Wisconsin · US

Funding

Research ServicesP01HL082798 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GREENE, ANDREW S. · 2006 to 2015
$22.0M
RESEARCH TRAINING IN HEMATOLOGYT32HL007899 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Jane Ellen Churpek · 1998 to 2026
$8.2M
Inflammation and Infection in Acquired & Congenital Cardiovascular DiseaseT32HL094273 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GREENE, ANDREW S. · 2009 to 2013
$850k
NHLBI NIH HHS HL-082798NHLBI NIH HHS P01 HL082798NHLBI NIH HHS T32 HL007899NHLBI NIH HHS T32HL-094273
6 · The paper itself

Abstract

Bone marrow-derived endothelial progenitor cells (BM-EPCs) are stimulated by vascular endothelial growth factor-A (VEGF-A) and other potent proangiogenic factors. During angiogenesis, an increase in VEGF-A expression stimulates BM-EPCs to enhance endothelial tube formation and contribute to an increase in microvessel density. Hypoxia is known to produce an enhanced angiogenic response and heightened levels of VEGF-A have been seen in oxygen deprived epithelial and endothelial cells, yet the pathways for VEGF-A signaling in BM-EPCs have not been described. This study explores the influence of hypoxia on VEGF-A signaling in rat BM-EPCs utilizing a novel proteomic strategy to directly identify interacting downstream components of the combined VEGF receptor(s) signaling pathways, gene expression analysis, and functional phenotyping. VEGF-A signaling network analysis following liquid chromatographic separation and tandem mass spectrometry revealed proteins related to inositol/calcium signaling, nitric oxide signaling, cell survival, cell migration, and inflammatory responses. Alterations in BM-EPC expression of common angiogenic genes and tube formation in response to VEGF-A during hypoxia were measured and combined with the proteomic analysis to enhance and support the signaling pathways detected. BM-EPC tube formation assays in response to VEGF-A exhibited little tube formation; however, a cell projection/migratory phenotype supported the signaling data. Additionally, a novel assay measuring BM-EPC incorporation into preformed endothelial cell tubes indicated a significant increase of incorporated BM-EPCs after pretreatment with VEGF-A during hypoxia. This study verifies known VEGF-A pathway components and reveals several unidentified mechanisms of VEGF-A signaling in BM-EPCs during hypoxia that may be important for migration to sites of vascular regeneration.

Indexed as

AnimalsBone Marrow CellsCell HypoxiaCell MovementCells, CulturedCell SurvivalChromatography, High Pressure LiquidEndothelial CellsGene Expression RegulationMass SpectrometryModels, GeneticNeovascularization, PhysiologicPeptide FragmentsProteomicsRatsRats, Sprague-DawleyPeptide FragmentsVascular Endothelial Growth Factor Avascular endothelial growth factor A (138-165)Vascular Endothelial Growth Factor Receptor-2endothelial progenitor cellshypoxiamass spectrometrysignalingvascular endothelial growth factor

Identifiers

PMID24022223
PMCPMC3841787
OpenAlexW2129818467

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.