Date of Graduation

12-2017

Document Type

Thesis

Degree Name

Bachelor of Science in Biomedical Engineering

Degree Level

Undergraduate

Department

Biomedical Engineering

Advisor

Balachandran, Kartik

Reader

Ravishankar, Prashanth

Abstract

Despite the high prevalence of calcific aortic valve disease (CAVD), the underlying mechanisms of pathogenesis have not been found yet. Therefore, it is extremely important to study CAVD and understand how it develops. For this matter, we decided to study the potential of endothelial progenitor cells (EPCs) for use in tissue-engineered models of heart valves. EPCs were chosen as the cell source of interest for this study due to their high neovascularization potential and use in regenerative medicine and cardiovascular tissue engineering.

In this project, we aimed to engineer the microenvironment of cells that are involved in the formation of heart valves. We hypothesized that cyclic strain induces EPCs to undergo differentiation, which will depend on the applied strain, culture media components and culture duration. EPCs isolated from human umbilical cord blood expressed endothelial cell markers CD31 and vascular endothelial growth factor receptor 2 (VEGFR2), and the progenitor cell marker CD34. The cells did not express the mesenchymal marker α-smooth muscle actin (α-SMA). EPCs showed an endothelial behavior demonstrated by the uptake of acetylated-low density lipoprotein (Dil-Ac-LDL), and a vasculogenic potential demonstrated by tube formation. The cells were subjected to 20% strain rates by utilizing a cyclic uniaxial biostretcher for 7 days and showed a mild expression of α-SMA. Considering these events, EPCs were subjected to 20% strain for longer periods of time (1, 2, and 3 weeks) and showed maintained CD31 expression, no α-SMA expression, and increased CD34 expression suggesting an increased vascular-like behavior after strain.

Keywords

Developmental Biology, Endothelial progenitor cells, blood mononuclear cells, tissue engineering, umbilical cord blood

Available for download on Saturday, May 25, 2019

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