ArticleBiomechanics and modeling in mechanobiology2023
Impact of spatial and temporal stability of flow vortices on vascular endothelial cells.
Article in Biomechanics and modeling in mechanobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Computational Modeling Meets 3D Bioprinting: Emerging Synergies in Cardiovascular Disease Modeling.Advanced healthcare materials · 2026Review
- Artificial intelligence-based machine learning protocols enable quicker assessment of aortic biomechanics: A case study.Journal of vascular surgery cases and innovative techniques · 2025Article
- Improving rupture status prediction for intracranial aneurysms using wall shear stress informatics.Acta neurochirurgica · 2025Article
- Fluid-Dynamic Modeling of Flow in Embryonic Tissue Indicates That Lymphatic Valve Location Is Not Consistently Determined by the Local Fluid Shear or Its Gradient.Microcirculation (New York, N.Y. : 1994) · 2024Article
- Characterization of small abdominal aortic aneurysms' growth status using spatial pattern analysis of aneurismal hemodynamics.Scientific reports · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
purposeIntracranial aneurysms (IAs) are pathological dilations of cerebrovascular vessels due to degeneration of the mechanical strength of the arterial wall, precluded by altered cellular functionality. The presence of swirling hemodynamic flow (vortices) is known to alter vascular endothelial cell (EC) morphology and protein expression indicative of IAs. Unfortunately, less is known if vortices with varied spatial and temporal stability lead to differing levels of EC change. The aim of this work is to investigate vortices of varying spatial and temporal stability impact on ECs.
methodsVortex and EC interplay was investigated by a novel combination of parallel plate flow chamber (PPFC) design and computational analysis. ECs were exposed to laminar (7.5 dynes/[Formula: see text] wall shear stress) or low (<1 dynes/[Formula: see text]) stress vortical flow using PPFCs. Immunofluorescent imaging analyzed EC morphology, while ELISA tests quantified VE-cadherin (cell-cell adhesion), VCAM-1 (macrophage-EC adhesion), and cleaved caspase-3 (apoptotic signal) expression. PPFC flow was simulated, and vortex stability was calculated via the temporally averaged degree of (volume) overlap (TA-DVO) of vortices within a given area.
resultsEC morphological changes were independent of vortex stability. Increased stability promoted VE-cadherin degradation (correlation coefficient r = [Formula: see text]0.84) and 5-fold increased cleaved caspase-3 post 24 h in stable (TA-DVO 0.736 ± 0.05) vs unstable (TA-DVO 0.606 [Formula: see text]0.2) vortices. ECs in stable vortices displayed a 4.5-fold VCAM-1 increase than unstable counterparts after 12 h.
conclusionThis work demonstrates highly stable disturbed flow imparts increased inflammatory signaling, degraded cell-cell adhesion, and increased cellular apoptosis than unstable vortices. Such knowledge offers novel insight toward understanding IA development and rupture.
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