Poster # 1
MODELING DIABETIC ENDOTHELIAL CELL DYSFUNCTION IN VITRO
Authors: Rayyan Gorashi and Bin Jiang, Northwestern University
PRESENTER’S INFO:
Name: Rayyan Gorashi
Email: rayyangorashi2021@u.northwestern.edu
Title: Student
Affiliation: Northwestern University
Department: Biomedical Engineering
Advisor: Dr. Bin Jiang
Advisor’s Email: bin.jiang@northwestern.edu
NOTE: This poster will also be presented during the symposium Twitter Poster Session on the day of the symposium, Friday, October 30 between 9:00 – 11:30 AM (CT). Twitter posters will be available all day for viewing and interactive discussions. Posters will remain viewable on Twitter through the weekend from October 31-November 1.
Twitter Handle: @RayyanGo
Abstract: Diabetes is one of the major risk factors for cardiovascular diseases, which is mediated with vascular endothelial dysfunction. Currently, there is no in vitro disease model of endothelial cell dysfunction in diabetic patients, which hinders mechanistic understanding and therapeutic discovery. Our model utilizes induced pluripotent stem cell derived endothelial cells from healthy patients and patients diagnosed with diabetes and peripheral arterial disease. The conditions of diabetes result in increased oxidative stress on the endothelial cells, ultimately compromising their barrier function and allowing for increased endothelial permeability, leading to the development of various cardiovascular complications. Diabetic patients also have chronic inflammation, allowing for increased risk of development of thrombosis. We identified four categories of assessment for endothelial cell dysfunction: oxidative stress, inflammation, permeability, and thrombosis. To simulate in situ conditions of diabetes, we incorporated hyperglycemic (25 mM glucose) and high urea (20 mM) conditions into our model. Overall, the qualitative effect of the high glucose and high urea treatment group resulted in the most apparent effect on permeability, while the high urea group appeared to strengthen membrane expression for surface adhesion molecules involved in inflammation. In future experiments, hyperlipidemia will be incorporated into the experimental design. The development of a robust in vitro model of diabetic endothelial dysfunction, similar to the onset of type II diabetes, will allow for high-throughput testing of pharmacological agents to ultimately treat the disease’s effects within the vascular bed. The widespread implications of type II diabetes on the vascular bed further amplify the significance of this study in the development of pharmacological agents to treat the disease.
Audio presentation:
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