Evidence map›Paper›PMID 30681366›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2019

Activation of Notch signaling by soluble Dll4 decreases vascular permeability via a cAMP/PKA-dependent pathway.

Rachel Boardman, Vincent Pang, Naseeb Malhi, Amy P Lynch, Lopa Leach, Andrew V Benest, David O Bates, Maria J C Machado

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. GFAPProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. YAP/TAZ drives Notch and angiogenesis mechanoregulation in silico.NPJ systems biology and applications · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. 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

8 authors at 2 institutions in 1 country.

Rachel BoardmanCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Vincent PangCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Naseeb MalhiCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Amy P LynchCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Lopa LeachDivision of Physiology Pharmacology and Neuroscience, School of Life Sciences, The Medical School , Nottingham , United Kingdom.
Andrew V BenestCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
David O BatesCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Maria J C MachadoCancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham , Nottingham , United Kingdom.
Queen's Medical Centre · GBUniversity of Nottingham · GB

Funding

British Heart Foundation PG/11/67/29067British Heart Foundation PG/13/85/30536British Heart Foundation PG/18/31/33759Medical Research Council 1361718Medical Research Council MR/K013157/1
6 · The paper itself

Abstract

The Notch ligand delta-like ligand 4 (Dll4), upregulated by VEGF, is a key regulator of vessel morphogenesis and function, controlling tip and stalk cell selection during sprouting angiogenesis. Inhibition of Dll4 results in hypersprouting, nonfunctional, poorly perfused vessels, suggesting a role for Dll4 in the formation of mature, reactive, functional vessels, with low permeability and able to restrict fluid and solute exchange. We tested the hypothesis that Dll4 controls transvascular fluid exchange. A recombinant protein expressing only the extracellular portion of Dll4 [soluble Dll4 (sDll4)] induced Notch signaling in endothelial cells (ECs), resulting in increased expression of vascular-endothelial cadherin, but not the tight junctional protein zonula occludens 1, at intercellular junctions. sDll4 decreased the permeability of FITC-labeled albumin across EC monolayers, and this effect was abrogated by coculture with the γ-secretase inhibitor

Indexed as

Adaptor Proteins, Signal TransducingAdherens JunctionsAnimalsAntigens, CDCadherin 5CadherinsCalcium-Binding ProteinsCapillary PermeabilityCells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesHumansHuman Umbilical Vein Endothelial CellsMaleMesenteryProtein Kinase InhibitorsAdaptor Proteins, Signal TransducingAntigens, CDCadherin 5CadherinsCalcium-Binding ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesDLL4 protein, humanProtein Kinase InhibitorsReceptors, Notchdelta-like ligand 4endothelial cellsNotchvascular permeability

Identifiers

PMID30681366
PMCPMC6580391
OpenAlexW2912549196

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.