Evidence map›Paper›PMID 20054616›Full record

ArticleMolecular and cellular biochemistry2010

Sprouty1 inhibits angiogenesis in association with up-regulation of p21 and p27.

Sangjin Lee, Tri M Bui Nguyen, Dmitry Kovalenko, Neeta Adhikari, Suzanne Grindle, Sean P Polster, Robert Friesel, Sundaram Ramakrishnan, Jennifer L Hall

Abstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  11. SOX7 Target Genes and Their Contribution to Its Tumor Suppressive Function.International journal of molecular sciences · 2018
    Article
  12. Article
  13. Fibroblast growth factor signaling in the vasculature.Current atherosclerosis reports · 2015
    Review
  14. Development and pathologies of the arterial wall.Cellular and molecular life sciences : CMLS · 2014
    Review
  15. Human Sprouty1 suppresses growth, migration, and invasion in human breast cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  16. Article
  17. Article
  18. 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

9 authors at 3 institutions in 1 country.

Sangjin LeeLillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA.
Tri M Bui Nguyen
Dmitry Kovalenko
Neeta Adhikari
Suzanne Grindle
Sean P Polster
Robert Friesel
Sundaram Ramakrishnan
Jennifer L Hall
University of Minnesota · USMaine Medical Center · USMinneapolis Heart Institute Foundation · US

Funding

Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
Regulation of Endothelial Cell Function by SproutyR01HL065301 · NHLBI · MAINE MEDICAL CENTER · PI FRIESEL, ROBERT E · 2001 to 2010
$2.0M
NCRR NIH HHS P20 RR015555NCRR NIH HHS P20 RR15555NHLBI NIH HHS R01 HL065301NHLBI NIH HHS R01 HL65301
6 · The paper itself

Abstract

Sprouty1 (Spry1) is a conserved antagonist of FGF signaling. The goal of this study was to further explore the downstream mechanisms governing Spry1 inhibition of endothelial cell proliferation. Up-regulation of Spry1 in HUVECs inhibited tube formation on Matrigel (n = 6, P < 0.001). This was associated with decreased proliferation as measured by BrdU incorporation (n = 6, P < 0.001) and increased protein expression of the cyclin-dependent kinase inhibitor 1A (CDKN1A), p21 and cyclin-dependent kinase inhibitor 1B (CDKN1B), p27. A transcriptional analysis using a targeted human angiogenesis array following up-regulation of Spry1 demonstrated a >2-fold increase in an anti-angiogenic factor, serpin peptidase inhibitor, clad F (Serpinf1), and a >2-fold decrease in pro-angiogenic factors fms-related tyrosine kinase 1 (FLT1), angiopoietin2 (Ang-2), and placental growth factor (PGF) (n = 2). To define upstream mechanisms that may regulate endogenous Spry1, we performed a search for responsive elements upstream of the promoter region. This search resulted in the identification of multiple degenerate hypoxia responsive elements. Exposure to hypoxia resulted in a significant increase in Spry1 expression (n = 8, P < 0.01). These findings shed new light on downstream signaling pathways associated with Spry1 anti-proliferative responses, and provide new evidence that hypoxia stimulates Spry1 expression.

Indexed as

Neovascularization, PhysiologicCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Endothelial CellsHumansHypoxiaMembrane ProteinsPhosphoproteinsPromoter Regions, GeneticRNA, MessengerSignal TransductionUp-RegulationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Membrane ProteinsPhosphoproteinsRNA, MessengerSPRY1 protein, human

Identifiers

PMID20054616
PMCPMC3334870
OpenAlexW2096945337

What OpenQuestion holds

Textmetadata
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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.