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Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
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EXPRESS: Post-stenotic hemodynamics in intracranial atherosclerosis are associated with endothelial activation and

Russell Nakasone1,2, Grace Prochilo1, Chuanlong Li1

  • 1David Geffen School of Medicine, Departments of Neurology, The University of California, Los Angeles, Los Angeles, CA, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|August 12, 2026
PubMed

Insights

Low wall shear stress in narrowed brain arteries promotes endothelial cell growth and pro-thrombotic activity, contributing to stroke risk in intracranial atherosclerotic disease (ICAD).

Area of Science:

  • Cerebrovascular disease
  • Biomedical engineering
  • Translational medicine

Background:

  • Intracranial atherosclerotic disease (ICAD) is a major cause of ischemic stroke.
  • The role of post-stenotic cerebral hemodynamics in endothelial dysfunction is not well understood.
  • This study investigates the link between low wall shear stress (WSS) and endothelial changes in middle cerebral artery (MCA) stenoses.

Purpose of the Study:

  • To determine if focal post-stenotic low WSS in patient-specific MCA stenoses is associated with endothelial proliferation and pro-thrombotic activation.
  • To explore the relationship between hemodynamic forces and endothelial cell behavior in the context of ICAD.

Main Methods:

  • Computational fluid dynamics (CFD) analysis of CTA-derived geometries from 33 paired MCAs.
  • 3D printing of stenotic and control MCA models for endothelial cell perfusion studies.
  • Confocal imaging and automated segmentation to analyze endothelial proliferation (Ki-67), biglycan (BGN) expression, cell morphology, and pro-thrombotic mediators (LPCAT2, PAI1).

Main Results:

  • Stenotic MCAs showed significantly larger low-WSS areas compared to controls.
  • Low-WSS regions were associated with increased endothelial proliferation and BGN expression.
  • Low-WSS environments exhibited reduced cell area and elevated LPCAT2 and PAI1 expression, indicating pro-thrombotic signaling.

Conclusions:

  • Patient-specific cerebral stenoses create focal low-WSS areas.
  • These low-WSS environments can drive endothelial proliferation and pro-thrombotic signaling.
  • This supports a mechanistic link between intracranial hemodynamics and endothelial dysfunction in ICAD.
Abstract

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