Date of Award

8-2015

Document Type

Thesis

Degree Name

Master of Science (MS)

Legacy Department

Bioengineering

Advisor

LaBerge, Martine

Committee Member

Simionescu, Dan

Abstract

Vascular complications are the leading cause of morbidity and mortality amongst diabetic patients which represent a major proportion of patients undergoing coronary artery revascularization. Major advances in drug eluting stent technologies have reduced the overall rates of restenosis in general however diabetic patients still remain at a high risk thus requiring target lesion revascularization more commonly as compared to non-diabetic cohort. Phenotypic modulation demonstrated by smooth muscle cells is essential for normal wound healing response however is also contributive to initiation and development of various vascular complications including neointimal hyperplasia which ultimately leads to the lumen re-narrowing or restenosis. Hyperglycemia is the hallmark of diabetes with clinical evidence of poor glycemic control correlated with exaggerated neointimal hyperplasia. Although the contribution of phenotypic modulation to the development of restenosis has been well explored nevertheless, our understanding of this characteristic response in diabetic patients remains less understood. In the current study, the effects of acute and chronic hyperglycemia on vascular smooth muscle cell phenotypic modulation under mechanically loaded conditions were evaluated and current results suggests an exaggerated response in acute and chronic conditions. The long term goal of this project is to design an in vitro dynamic disease model which would compare cellular response to combined hemodynamic disturbances and metabolic abnormalities thus elucidating novel drug and targets aimed at reducing neointimal hyperplasia in diabetic patients.

Included in

Engineering Commons

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