Evidence map›Paper›PMID 23393387›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2013

Thioredoxin-interacting protein mediates sustained VEGFR2 signaling in endothelial cells required for angiogenesis.

Shin-Young Park, Xi Shi, Jinjiang Pang, Chen Yan, Bradford C Berk

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cytoskeletal Remodeling Mimics Endothelial Response to Microgravity.Frontiers in cell and developmental biology · 2021
    Article
  5. Article
  6. Redox RegulationAntioxidants & redox signaling · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Shin-Young ParkAab Cardiovascular Research Institute, University of Rochester, 601 Elmwood Ave, Box CVRI, Rochester, NY 14642, USA.
Xi Shi
Jinjiang Pang
Chen Yan
Bradford C Berk
University of Rochester · US

Funding

Flow Responsive Mediators of Inflammation and SurvivalR01HL106158 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C, YAN, CHEN · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL106158
6 · The paper itself

Abstract

objectiveThioredoxin-interacting protein (TXNIP) is an α-arrestin protein whose function is important for the regulation of vascular endothelial growth factor receptor 2 (VEGFR2) signaling and endothelial cell survival. Because VEGFR2 is critical for angiogenesis, we explored the role of TXNIP in VEGF-induced angiogenesis. APPROACH AND

resultsTXNIP knockdown inhibited VEGF-induced endothelial cell tube formation and proliferation in cultured human umbilical vein endothelial cell. To elucidate the mechanism by which TXNIP altered VEGFR2 signaling in human umbilical vein endothelial cell, we studied phosphorylation of VEGFR2, phospholipase C gamma-1 (PLCγ1), endothelial NO synthase, and Akt (known as protein kinase B). TXNIP knockdown significantly decreased phosphorylation of VEGFR2 and PLCγ1 at times >5 minutes, but phosphorylation was unchanged at 2 minutes, as was Akt and endothelial NO synthase phosphorylation. Cell-surface biotinylation assay showed that TXNIP knockdown significantly attenuated VEGFR2 internalization. These results suggested that TXNIP was required for sustained VEGFR2 signaling, which is mediated largely by internalized VEGFR2. Rab5 knockdown to inhibit the trafficking and fusion of early endosomes significantly blocked VEGF-induced VEGFR2 internalization and phosphorylation of VEGFR2 and PLCγ1. Immunofluorescence and coimmunoprecipitation showed that TXNIP was part of a complex that included Rab5 and VEGFR2. Finally, TXNIP knockdown prevented the association of VEGFR2 and Rab5.

conclusionsOur results show that TXNIP is essential for VEGFR2 internalization in Rab5 positive endosomes, which is required for endothelial cell growth and angiogenesis.

Indexed as

Neovascularization, PhysiologicSignal TransductionBiotinylationCarrier ProteinsCell MovementCell ProliferationCells, CulturedEndosomesFluorescent Antibody TechniqueHumansHuman Umbilical Vein Endothelial CellsImmunoprecipitationMicroscopy, FluorescenceNitric Oxide Synthase Type IIIPhospholipase C gammaPhosphorylationCarrier ProteinsNitric Oxide Synthase Type IIINOS3 protein, humanPhospholipase C gammaPLCG1 protein, humanProto-Oncogene Proteins c-aktrab5 GTP-Binding ProteinsTXNIP protein, humanVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID23393387
PMCPMC3629821
OpenAlexW2138168819

What OpenQuestion holds

Textmetadata
LicenceTDM
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.