Evidence map›Paper›PMID 42348369›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2026

ZEB1 Modifies VE-Cadherin Signaling in Lymphatic Endothelial Cells.

Nada S Ahmed, Joseph L Horder, Charles T Cresswell, Poppy E Harris, Amy P Lynch, Zarah B Tabrizi, Kathryn R Green, James H Hallwood, Anton C Smith, Michael A Portelli and 8 more

Abstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Nada S AhmedEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Joseph L HorderEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Charles T CresswellEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Poppy E HarrisEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Amy P LynchTumour Vascular Biology Laboratories, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Zarah B TabriziEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Kathryn R GreenEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
James H HallwoodTumour Vascular Biology Laboratories, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Anton C SmithTumour Vascular Biology Laboratories, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Michael A PortelliCentre for Respiratory Research, National Institute for Health Research Nottingham Biomedical Research Centre, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.ORCID 0000-0003-0821-4575
Alexander J FezovichHypoxia and Acidosis Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Christos SpanosWellcome Discovery Research Platform for Hidden Cell Biology, University of Edinburgh, Edinburgh, UK.
David S GardnerSchool of Veterinary Medicine and Science, University of Nottingham, Nottingham, UK.ORCID 0000-0002-6490-2412
Alan McIntyreHypoxia and Acidosis Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.ORCID 0000-0002-4791-7292
Sarah J StorrNottingham Breast Cancer Research Centre, School of Medicine, University of Nottingham, Biodiscovery Institute, University Park, UK.
Daniel G BoothCell Division and Chromosome Structure Laboratory, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
David O BatesTumour Vascular Biology Laboratories, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Andrew V BenestEndothelial Quiescence Group, Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.ORCID 0000-0002-8225-5159

Funding

BBSRC BB/V005626/1British Heart Foundation AVB/DOB PG/18/31/33759, PG/22/10913, PG/21/10796Wellcome Trust 2183052/19/ZWellcome Trust DTP 218466/Z/19/Z
6 · The paper itself

Abstract

objectiveZinc finger E-box-binding homeobox 1 (ZEB1) is a transcription factor primarily known for its regulatory roles in epithelial-to-mesenchymal transition (EMT) and cell fate determination. Recent studies suggest that endothelial ZEB1 signaling promotes blood vessel growth and reduces junctional integrity, although the underlying mechanisms remain unclear. Notably, the role of ZEB1 in the lymphatic vasculature is unknown, and the regulation of lymphatic integrity by VE-cadherin remains poorly defined.

methodsHere, using an integrated proteomic and transcriptomic approach, we identify ZEB1-dependent signaling pathways associated with cell-cell junction reorganization in lymphatic endothelial cells (LECs).

resultsLoss of ZEB1 reduced VE-cadherin phosphorylation at pY731 and pY685 and was accompanied by decreased monolayer resistance and impedance, together with increased leukocyte transendothelial migration. ZEB1 knockdown also reduced YES tyrosine kinase expression and altered YAP1 expression and junctional localisation, changes that were associated with reduced VE-cadherin phosphorylation. Silencing YAP1 in HDLECs similarly reduced VE-cadherin phosphorylation and impaired barrier integrity, recapitulating aspects of the phenotype observed following ZEB1 knockdown.

conclusionsCollectively, these findings suggest that ZEB1 contributes to lymphatic endothelial barrier maintenance in association with altered YAP1 and YES signaling.

Indexed as

Antigens, CDCadherinsEndothelial CellsSignal TransductionZinc Finger E-box-Binding Homeobox 1AnimalsCadherin 5HumansPhosphorylationYAP-Signaling ProteinsAntigens, CDCadherin 5CadherinsYAP-Signaling ProteinsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID42348369
PMCPMC13297878

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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.