The role of elastic fibers in soft tissues has been recognized as the material that provides distensibility and elasticity, where that of collagen fibers is to prevent deformation. The highly nonlinear stress-strain behavior of mammalian ascending aorta (AA) has long been seen as the result of elastin fiber in low strain region and collagen in high strain region. By conducting passive biaxial mechanical testing on newborn mice aorta, we are able to see the difference in mechanical behavior of aorta with FBLN 4 (Fibulin 4) -/- and LOX (Lysyl Oxidase) -/-. FBLN 4 is considered to play a role in elastin formation, and LOX in elastin cross linking. Mice with FBLN 4 -/- and LOX -/- die immediately after birth with tortuous aorta , fragmented elastin, and severe lung and aortic defects. Mice that underexpress FBLN 4 and LOX develop hypertension. Our results indicate that the stiffness for LOX -/- and FBLN 4 -/- under in vivo pressure is higher on average but is not significantly different from their wild type counterparts, indicating that hypertension is a remodeling mechanism of mice that under-express LOX or FBLN 4 to adapt to hemodynamic conditions. Our results also show that FBLN 4 -/- are less capable of storing energy in the loading cycle than their wild type counterparts, whereas LOX -/- are as capable as their wild type counterparts. This differentiation between samples indicates that albeit both types of genetic knockout samples result in fragmentation of elastin fiber, they also produce more subtle yet different changes in arterial structural integrity that must be further investigated.

Document Type

Final Report

Author's School

McKelvey School of Engineering

Author's Department

Mechanical Engineering and Materials Science

Class Name

Mechanical Engineering and Material Sciences Independent Study

Date of Submission