In vascular regions where blood flow is laminar, the endothelial cells that line the inner vessel wall are healthy and the vessel is protected from disease. Disturbed flow, which is low and reciprocating, coincides with dysfunctional endothelial cells and atherosclerotic plaque. The conversion of flow stimuli into endothelial biological events is defined as endothelial mechanotransduction. To increase our understanding of the means by which endothelial cell mechanotransduction occurs in order to prevent or promote atherosclerosis, Professor Ebong and her research group are applying chemical engineering, bioengineering, and biology to study the structure and function of the endothelial cell surface glycocalyx (sugar coat) that directly interfaces with flowing blood and sheds in the presence of atherosclerosis. Previously, it was shown that the endothelial cell surface glycocalyx plays a role in laminar flow-induced nitric oxide release, cytoskeleton reorganization, cell-cell junction changes, and cell shape remodeling. Moving the field forward, Professor Ebong and her research group are using fluorescent intracellular biomarkers, fluorescence confocal microscopy, protein biochemistry, RNA interference techniques, cryopreservation, and electron microscopy to define the ultrastructure of the endothelial surface glycocalyx, its changes as a result of the macro- or micro-vessel origin and due to the bio-chemical and -mechanical environment, glycocalyx mechanisms of mechanobiology, and the role of the glycocalyx in vascular health or disease. In vivo studies are performed using high fat fed apolipoprotein E (ApoE) knockout mice, a well established animal model of cardiovascular disease, to determine which glycocalyx components can be targeted to prevent, diagnose, or treat atherosclerosis (underlies a number of cardiovascular conditions), metastatic cancer, and leaky blood-brain barrier issues related to neurodegenerative diseases.