02/23/2026
By Dongming Xie
Day: Thursday, Feb. 26
Time: 3:30-4:45 p.m.
Location: Shah Hall 303
Abstract: Mechanical forces generated by blood flow and transmitted through the vessel wall play a decisive role in cardiovascular health and disease. Endothelial cells, which form the inner lining of all blood vessels, rely on the endothelial glycocalyx, a nanoscale, gel‑like layer of sugars and proteins, to sense these forces and convert them into biochemical signals that maintain vascular stability. Disruption of this structure is increasingly recognized as a central driver of vascular dysfunction. To investigate how mechanical environments regulate glycocalyx integrity and endothelial behavior, engineered in vitro systems are combined with in vivo models. These experimental platforms integrate controlled fluid flow, tunable substrate stiffness, and mammalian endothelial cells to recreate protective and pathological mechanobiological conditions. This framework enables systematic examination of how stagnation or disturbed flow at vessel branch points, hypertension‑associated tissue stiffening, and other mechanical cues alter glycocalyx structure, mechanotransduction pathways, barrier function, vascular tone, and intercellular signaling. Results demonstrate that mechanical perturbations promote glycocalyx degradation, leading to breakdown of endothelial barrier integrity, dysregulation of vascular tone, and disruption of key signaling pathways. These mechanobiological changes accelerate atherosclerotic plaque development, increase cancer cell adhesion and transendothelial migration, and exacerbate vascular dysfunction implicated in neurodegenerative disease. Complementary in vivo studies confirm the physiological relevance of these findings. Overall, this body of work establishes the glycocalyx as a mechanically sensitive regulator of vascular health and a potential therapeutic target aimed at restoring endothelial function across cardiovascular, cancer, and neurological contexts.