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August 20, 2025APL BioengineeringOpen Access

Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study

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Authors

PBPranav Vasanthi BathrinarayananTAThomas AbadiePEPatricia Pérez Esteban

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Overview

Observation shows elevated hydrostatic pressure disrupts VE-cadherin in endothelial cells, indicating mechanosensitive channels' role.

Key Points

  • Elevated hydrostatic pressure disrupts VE-cadherin dynamics at cell–cell junctions over time.
  • 1-hour exposure at high shear stress triggered formation of projections; low shear stress showed no effect.
  • Microfluidic organ-on-chip platform enabled analysis of mechanotransduction effects on endothelial cells.
  • Prolonged exposure to low shear pressure caused junction disruption, reversible with channel inhibition.

Cite This Study

Bathrinarayanan et al. (2025) studied this question.

synapsesocial.com/papers/68af3e49cf1dd9ea359eb567https://doi.org/10.1063/5.0275985
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Also Consider

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  1. 1A critical role for VE-cadherin in regulating actin dynamics during endothelial maturation and non-inflammatory activation via a tension-sensitive intermediate state2025
  2. 2Pressure Points: Endothelial Responses to Shear Stress and Pressure in Health and Pulmonary Arterial Hypertension2025
  3. 3Elucidating the mechanosensitive pathways of physiological and pathological strain on valve cells in a novel human valve-on-chip system2025
  4. 4Comparative Analysis of the Endothelial Glycocalyx in Aortic Valve and Vascular Endothelial Cells Under Distinct Shear Stress Conditions2025
  5. 5The Notch1 intracellular domain orchestrates mechanotransduction of fluid shear stress2025