Date of Award

1-1-2015

Language

English

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

College/School/Department

Department of Nanoscale Science and Engineering

Program

Nanoscale Sciences

Content Description

1 online resource (xi, 96 pages) : color illustrations

Dissertation/Thesis Chair

Susan Sharfstein

Committee Members

Susan Sharfstein, Yubing Xie, John Danias, Sarah Brenner, Mark Stewart

Keywords

3D, drug screening, extracel, Glaucoma, tissue engineering, High throughput screening (Drug development), Aqueous humor, BioMEMS, Microfluidic devices

Subject Categories

Biomedical Engineering and Bioengineering | Engineering

Abstract

Among ocular pathologies, glaucoma remains the second leading cause of blindness. The molecular mechanisms that lead to glaucoma have been attributed to damage of the conventional outflow tract. Conventional outflow tissues, a composite of the trabecular meshwork and the Schlemm's canal, regulate and maintain homeostatic responses of aqueous humor outflow. In glaucoma, drainage of aqueous humor into the Schlemm's canal is hindered, leading to an increase in intraocular pressure (IOP). That increase in IOP is directly correlated with retinal ganglion cell death, eliminating the relay of visual information to the thalamus and visual cortex, leading to blindness. Although disturbance in the conventional outflow tract has been implicated as the cause of glaucoma, a mechanism remains to be elucidated. In addition, there are no drugs targeting this structure implicated as the cause of glaucoma. This is, in part, due to limits in our understanding of the pathology at the molecular level and lack of an in vitro model system for outflow studies. Currently, anterior segments of animal or human cadaver eyes are used to study the outflow facility and test the effects of medications on the trabecular meshwork (TM), but these perfusions are cumbersome and expensive, making them impractical for high-throughput screening.

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