Author

Thomas Abadie

University of BirminghamORCID 0000-0002-4338-2948Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

Daniele VigoloiD· 2 shared Liam Michael GroveriD· 2 shared Mark J.H. SimmonsiD· 2 shared Pranav Vasanthi BathrinarayananiD· 2 shared Patricia Pérez EstebaniD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

5 top collaborators · 10 mutual co-author links

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2 shared papersBioengineering

Daniele VigoloORCID

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2 papers

Recent·Most cited

Elevated hydrostatic pressure modulates endothelial junctional mechanotransduction through VE-cadherin remodelling and altered association with YAP1, EPS8: an endothelium-on-chip study

Pranav Vasanthi Bathrinarayanan, Thomas Abadie, Daniele Vigolo, Mark J.H. Simmons, Liam Michael Grover

This study investigates how elevated hydrostatic pressure affects endothelial junctions using an endothelium-on-chip model, revealing changes in VE-cadherin structure, YAP1 localization, and EPS8 interactions.

bioRxiv · Sep 1, 2026 · PreprintBioengineering

Elevated hydrostatic pressure acts via piezo-1 to destabilise VE-cadherin junctions: an endothelium-on-chip study

Pranav Vasanthi Bathrinarayanan, Thomas Abadie, Patricia Pérez Esteban, Daniele Vigolo, Mark J.H. Simmons, Liam Michael Grover

This study shows elevated hydrostatic pressure affects VE-cadherin junctions via piezo-1, with effects dependent on shear stress duration and intensity.

bioRxiv · Mar 27, 2025 · PreprintBioengineering