YAP/TAZ drives Notch and angiogenesis mechanoregulation in silico.


Journal

NPJ systems biology and applications
ISSN: 2056-7189
Titre abrégé: NPJ Syst Biol Appl
Pays: England
ID NLM: 101677786

Informations de publication

Date de publication:
05 Oct 2024
Historique:
received: 30 04 2024
accepted: 22 09 2024
medline: 6 10 2024
pubmed: 6 10 2024
entrez: 5 10 2024
Statut: epublish

Résumé

Endothelial cells are key players in the cardiovascular system. Among other things, they are responsible for sprouting angiogenesis, the process of new blood vessel formation essential for both health and disease. Endothelial cells are strongly regulated by the juxtacrine signaling pathway Notch. Recent studies have shown that both Notch and angiogenesis are influenced by extracellular matrix stiffness; however, the underlying mechanisms are poorly understood. Here, we addressed this challenge by combining computational models of Notch signaling and YAP/TAZ, stiffness- and cytoskeleton-regulated mechanotransducers whose activity inhibits both Dll4 (Notch ligand) and LFng (Notch-Dll4 binding modulator). Our simulations successfully mimicked previous experiments, indicating that this YAP/TAZ-Notch crosstalk elucidates the Notch and angiogenesis mechanoresponse to stiffness. Additional simulations also identified possible strategies to control Notch activity and sprouting angiogenesis via cytoskeletal manipulations or spatial patterns of alternating stiffnesses. Our study thus inspires new experimental avenues and provides a promising modeling framework for further investigations into the role of Notch, YAP/TAZ, and mechanics in determining endothelial cell behavior during angiogenesis and similar processes.

Identifiants

pubmed: 39368976
doi: 10.1038/s41540-024-00444-3
pii: 10.1038/s41540-024-00444-3
doi:

Substances chimiques

Receptors, Notch 0
YAP-Signaling Proteins 0
Transcription Factors 0
Adaptor Proteins, Signal Transducing 0
YAP1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

116

Subventions

Organisme : EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions)
ID : 846617
Organisme : Wellcome Trust
ID : FC001751
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001751
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001751
Pays : United Kingdom

Informations de copyright

© 2024. The Author(s).

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Auteurs

Margot Passier (M)

Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands.
Institute for Complex Molecular Systems (ICMS), Eindhoven University of Technology, Eindhoven, the Netherlands.

Katie Bentley (K)

The Francis Crick Institute, London, UK.
Department of Informatics, King's College London, London, UK.

Sandra Loerakker (S)

Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands.
Institute for Complex Molecular Systems (ICMS), Eindhoven University of Technology, Eindhoven, the Netherlands.

Tommaso Ristori (T)

Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands. t.ristori@tue.nl.
Institute for Complex Molecular Systems (ICMS), Eindhoven University of Technology, Eindhoven, the Netherlands. t.ristori@tue.nl.

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