Evidence map›Paper›PMID 36740996›Full record

ArticleEMBO molecular medicine2023

Shear stress control of vascular leaks and atheromas through Tie2 activation by VE-PTP sequestration.

Keisuke Shirakura, Peter Baluk, Astrid F Nottebaum, Ute Ipe, Kevin G Peters, Donald M McDonald, Dietmar Vestweber

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
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  12. Review
  13. Review
  14. Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024
    Review
  15. Molecular Mechanisms Regulating Vascular Endothelial Permeability.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. MedComm · 2023
    Review
  20. Activin A Limits VEGF-Induced Permeability via VE-PTP.International journal of molecular sciences · 2023
    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

7 authors at 3 institutions in 2 countries.

Keisuke Shirakura *Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-9487-9495
Peter Baluk *Cardiovascular Research Institute, UCSF Helen Diller Family Comprehensive Cancer Center, and Department of Anatomy, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-2219-2616
Astrid F Nottebaum *Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0003-2246-7851
Ute IpeMax Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-8177-2680
Kevin G PetersAerpio Therapeutics, Inc., Blue Ash, OH, USA.ORCID 0000-0003-4717-4828
Donald M McDonaldCardiovascular Research Institute, UCSF Helen Diller Family Comprehensive Cancer Center, and Department of Anatomy, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-6985-9564
Dietmar VestweberMax Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-3517-732X
Max Planck Institute for Molecular Biomedicine · DEUniversity of California, San Francisco · USIo Therapeutics (United States) · US

Funding

ENDOTHELIAL PERMEABILITY IN AIRWAY ANGIOGENESISR01HL059157 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCDONALD, DONALD M · 1998 to 2015
$5.5M
Angiopoietin/Tie signaling regulation of vascular leakage in lung inflammationR01HL143896 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCDONALD, DONALD M · 2018 to 2021
$2.5M
Mechanisms, consequences, and reversal of abnormalities in lung lymphaticsR01HL127402 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCDONALD, DONALD M · 2015 to 2018
$2.2M
Deutsche Forschungsgemeinschaft (DFG) CRU342Deutsche Forschungsgemeinschaft (DFG) P2NHLBI NIH HHS R01 HL059157NHLBI NIH HHS R01 HL127402NHLBI NIH HHS R01 HL143896
6 · The paper itself

Abstract

Vascular endothelial protein tyrosine phosphatase (VE-PTP) influences endothelial barrier function by regulating the activation of tyrosine kinase receptor Tie2. We determined whether this action is linked to the development of atherosclerosis by examining the influence of arterial shear stress on VE-PTP, Tie2 activation, plasma leakage, and atherogenesis. We found that exposure to high average shear stress led to downstream polarization and endocytosis of VE-PTP accompanied by Tie2 activation at cell junctions. In aortic regions with disturbed flow, VE-PTP was not redistributed away from Tie2. Endothelial cells exposed to high shear stress had greater Tie2 activation and less macromolecular permeability than regions with disturbed flow. Deleting endothelial VE-PTP in VE-PTP

Indexed as

AtherosclerosisPlaque, AtheroscleroticAnimalsEndothelial CellsMiceReceptor-Like Protein Tyrosine Phosphatases, Class 3Receptor, TIE-2Receptor-Like Protein Tyrosine Phosphatases, Class 3Receptor, TIE-2aortaatherosclerosisendothelial junctionslaminar flowvascular leakage

Identifiers

PMID36740996
PMCPMC10086590
OpenAlexW4319294266

What Socratic 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 Socratic graph.