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BME Seminar: Dr. Eno Essien Ebong - Flow Conditions Stimulate Endothelial Mechanobiology to Prevent or Promote Disease

Event Date 

April 21, 2017 - 1:50pm


Wishnick Hall, Room 113
3255 South Dearborn
Chicago, IL 60616


Armour College of Engineering's Biomedical Engineering Department will host a seminar featuring Eno Essien Ebong, Assistant Professor, Department of Chemical Engineering and Bioengineering at Northeastern University on April 21, 2017. Lecture topic will be Flow Conditions Stimulate Endothelial Mechanobiology to Prevent or Promote Disease


The Ebong research lab studies how the mechanical forces of blood flow affect endothelial cells, which line the blood vessels and guard them from diseases like atherosclerosis—a pre¬cursor to heart attack and other serious conditions. Much of the focus is on studying the structure and function of the protective gel-like layer of sugar molecules and proteins coating the surface of the endothelial cells—called the glycocalyx—to understand, on a molecular level, how mechanobiology remodels the endothelial cells to facilitate protection from disease. This glycocalyx struc¬ture gives fragile arteries the resilience they need to with¬stand the rau¬cous fluid envi¬ron¬ment coursing through them, espe¬cially at the branch points where plaques are most prevalent. Glycocalyx sheds in the presence of atherosclerosis, so it is of great interest to study how gradual glycocalyx degradation initiates and/or promotes pathological remodeling that forms atherosclerotic lesions. The Ebong lab constructs in vitro systems comprising fluids and mammalian endothelial cells, to replicate both healthy and disruptive blood-flow conditions and to uncover the intricacies of the flow-glycocalyx-endothelial cell relationship. This work is combined with live animal studies to assess the validity of the findings, in real disease conditions. The long term goal is to leverage mechanobiology, endothelial cells, and the glycocalyx to develop therapies that reverse the progression of atherosclerosis.