Glycocalyx and Inflammation

Over the past several decades, it has been shown that the development of atherosclerosis, which had widely been associated as a consequence of high lipid levels, is, at least in some part, an inflammatory process. These discoveries have led to investigations on the effects of inflammation on the glycocalyx and found that inflammation may lead to degradation of the endothelial glycocalyx. The Ebong lab would like to further investigate inflammation and its effect on the glycocalyx by using high resolution imaging to determine the detailed structure of the glycocalyx pre- and post-inflammation.

Additionally, we hope to further elucidate the function of the glycocalyx in plaque development. Our aim is to study the interaction of the endothelium with oxidized low-density lipoproteins (oxLDLs), which are involved in the development of atherosclerotic plaques under varying glycocalyx conditions. More specifically, scavenger receptors on endothelial cells and macrophages recognize oxLDLs in the blood and induce foam cell formation and other inflammatory responses that lead to plaque formation. To determine the effects of the glycocalyx on plaque development, this project will analyze both an in vitro and an in vivo mouse MRI study. Using a flow chamber, we induce shear stress on a monolayer of rat fat pad endothelial cells and expose the cells to oxLDL. In the MRI studies, we are investigating the effects of endothelial injury on the uptake of oxLDL over a period of eight weeks. We hypothesize that endothelial cells with damaged or absent glycocalyx structures will allow a higher uptake of lipids than endothelial cells with healthy glycocalyx.