Evidence map›Paper›PMID 32369573›Full record

ArticleBlood2020

Platelets docking to VWF prevent leaks during leukocyte extravasation by stimulating Tie-2.

Laura J Braun, Rebekka I Stegmeyer, Kerstin Schäfer, Stefan Volkery, Silke M Currie, Birgit Kempe, Astrid F Nottebaum, Dietmar Vestweber

Abstract read
In one paragraph

Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Platelet effector functions in inflammation.Research and practice in thrombosis and haemostasis · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Direct mechanical exposure initiates hepatocyte proliferation.JHEP reports : innovation in hepatology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Platelets and (Lymph)angiogenesis.Cold Spring Harbor perspectives in medicine · 2023
    Review
  15. Article
  16. Platelets in COVID-19 disease: friend, foe, or both?Pharmacological reports : PR · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Laura J BraunMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Rebekka I StegmeyerMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Kerstin SchäferMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Stefan VolkeryMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Silke M CurrieMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Birgit KempeMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Astrid F NottebaumMax Planck Institute for Molecular Biomedicine, Münster, Germany.
Dietmar VestweberMax Planck Institute for Molecular Biomedicine, Münster, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophil extravasation requires opening of the endothelial barrier but does not necessarily cause plasma leakage. Leaks are prevented by contractile actin filaments surrounding the diapedesis pore, keeping this opening tightly closed around the transmigrating neutrophils. We have identified the receptor system that is responsible for this. We show that silencing, or gene inactivation, of endothelial Tie-2 results in leak formation in postcapillary venules of the inflamed cremaster muscle at sites of neutrophil extravasation, as visualized by fluorescent microspheres. Leakage was dependent on neutrophil extravasation, because it was absent upon neutrophil depletion. We identified the Cdc42 GTPase exchange factor FGD5 as a downstream target of Tie-2 that is essential for leakage prevention during neutrophil extravasation. Looking for the Tie-2 agonist and its source, we found that platelet-derived angiopoietin-1 (Angpt1) was required to prevent neutrophil-induced leaks. Intriguingly, blocking von Willebrand factor (VWF) resulted in vascular leaks during transmigration, indicating that platelets interacting with endothelial VWF activate Tie-2 by secreting Angpt1, thereby preventing diapedesis-induced leakiness.

Indexed as

Blood PlateletsAngiopoietin-1AnimalsCapillary PermeabilityHumansHuman Umbilical Vein Endothelial CellsLeukocytesMiceMice, Inbred C57BLReceptor, TIE-2Transendothelial and Transepithelial Migrationvon Willebrand FactorAngiopoietin-1Receptor, TIE-2von Willebrand Factor

Identifiers

PMID32369573
PMCPMC7413753

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.