Date of Award

8-2019

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Bioengineering

Committee Member

Naren Vyavahare, Committee Chair

Committee Member

Jiro Nagatomi

Committee Member

Agneta Simionescu

Abstract

Abdominal aortic aneurysms (AAA) are an area of dilation in the vessel that is greater than 3.0 cm in diameter or an area of the vessel that enlarged to greater than 50% of the vessel's original diameter. AAA are generally asymptomatic and if ruptured, have a mortality rate of 78-83%. AAA account for approximately 45,000 surgeries performed in the United States annually and are the 13th leading cause of death in the United States. Alterations of two extracellular matrix proteins, elastin and collagen, are associated with the formation of abdominal aortic aneurysms. AAA formation is marked by degradation of elastin and collagen induced by matrix metalloproteinases (MMPs) as well as a decrease in the amount of smooth muscle cells in the artery.

Elastase is the standard method of inducing an aneurysm in arterial tissue by breaking down the elastin fibers in the extracellular matrix. Numerous in vivo models have been published to induce the formation of an aneurysm using elastase, however there has yet to be model optimized in an ex vivo environment showing progressive AAA formation. An optimal ex vivo model is advantageous in the hopes of advancing aneurysmal research by studying abdominal aortic aneurysms through organ culture. This optimal ex vivo model should be consistent with previous in vivo models; diminished elastin content and smooth muscle cells and show presence of MMPs. Additionally, this model should minimize death of native cells in order to recapitulate an in vivo response and investigate the relationship between elastin damage and calcification. Therefore, our lab aims to produce an ex vivo model of elastase-induced elastin degradation in porcine carotid arteries that minimizes death of native cells.

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