Evidence map›Paper›PMID 21642504›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

Angiotensin II-induced process of angiogenesis is mediated by spleen tyrosine kinase via VEGF receptor-1 phosphorylation.

Cuneyt K Buharalioglu, Chi Young Song, Fariborz A Yaghini, Hafiz U B Ghafoor, Mustafa Motiwala, Tusita Adris, Anne M Estes, Kafait U Malik

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Review
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  11. Renin-angiotensin system and cancer: epidemiology, cell signaling, genetics and epigenetics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
  12. Article
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  17. Angiotensin II increases angiogenesis by NF-κB-mediated transcriptional activation of angiogenic factor AGGF1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  18. Article
  19. Review
  20. Article
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 1 institution in 1 country.

Cuneyt K BuharaliogluDepartment of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
Chi Young Song
Fariborz A Yaghini
Hafiz U B Ghafoor
Mustafa Motiwala
Tusita Adris
Anne M Estes
Kafait U Malik
University of Tennessee Health Science Center · US

Funding

Eicosanoid-Induced Vascular Growth During InjuryR01HL079109 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MALIK, KAFAIT U · 2005 to 2015
$3.3M
NHLBI NIH HHS R01 HL079109PHS HHS R01-079109-05
6 · The paper itself

Abstract

Spleen tyrosine kinase (Syk), expressed in endothelial cells, has been implicated in migration and proliferation and in vasculogenesis. This study was conducted to determine the contribution of Syk and the underlying mechanism to the angiogenic effect of ANG II and VEGF. Angiogenesis was determined by tube formation from the endothelial cell line EA.hy926 (EA) and human umbilical vein endothelial cells (HUVECs) and microvessel sprouting in rat aortic rings. ANG II (10 nM), EGF (30 ng/ml), and VEGF (50 ng/ml) stimulated EA cells and HUVECs to form tubular networks and increased aortic sprouting; these effects were blocked by VEGF receptor-1 and Flt-1 antibody (Flt-1/Fc) but not by the VEGF receptor-2 (Flk-1) antagonist SU-1498. ANG II increased the phosphorylation of Flt-1 but not Flk-1, whereas VEGF increased the phosphorylation of both receptors in EA cells and HUVECs. VEGF expression elicited by ANG II was not altered by Flt-1/Fc or SU-1498. EGF stimulated tube formation from EA cells and HUVECs and Flt-1 phosphorylation and aortic sprouting, which were blocked by the EGF receptor antagonist AG-1478 and Flt-1/Fc but not by SU-1498. ANG II-, EGF-, and VEGF-induced tube formation and aortic sprouting were attenuated by the Syk inhibitor piceatannol and by Syk short hairpin interfering (sh)RNA and small interfering RNA, respectively. ANG II, EGF, and VEGF increased Syk phosphorylation, which was inhibited by piceatannol and Syk shRNA in EA cells and HUVECs. Neither piceatannol nor Syk shRNA altered ANG II-, EGF-, or VEGF-induced phosphorylation of Flt-1. These data suggest that ANG II stimulates angiogenesis via transactivation of the EGF receptor, which promotes the phosphorylation of Flt-1 and activation of Syk independent of VEGF expression.

Indexed as

Neovascularization, PhysiologicAnalysis of VarianceAngiogenesis InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsCells, CulturedEndothelial CellsEnzyme ActivationEpidermal Growth FactorErbB ReceptorsHumansIntracellular Signaling Peptides and ProteinsPhosphorylationProtein Kinase InhibitorsProtein-Tyrosine KinasesAngiogenesis InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersEGFR protein, humanEgfr protein, ratEpidermal Growth FactorErbB ReceptorsFLT1 protein, humanFlt1 protein, ratIntracellular Signaling Peptides and ProteinsProtein Kinase InhibitorsProtein-Tyrosine KinasesSyk KinaseSYK protein, humanSyk protein, ratVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID21642504
PMCPMC3191073
OpenAlexW2097327255

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.