Journal of Clinical and Experimental Ophthalmology
Open Access
ISSN: 2155-9570
ISSN: 2155-9570
Cula N Dautriche
SUNY Polytechnic Institute, USA
Posters & Accepted Abstracts: J Clin Exp Ophthalmol
Among ocular pathologies, glaucoma remains the second leading cause of blindness. The exact molecular mechanisms that lead to glaucoma remain to be elucidated; yet 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. 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. To address this problem, we have successfully engineered a biomimetic conventional outflow tract as a model for understanding of TM outflow physiology and pathology and development of TM targeted therapies. We designed and used a 3D multi-culture system consisting of HTM cells and HSC cells sequentially seeded on a highly porous, micro-fabricated, hydrogel-scaffold. We demonstrated that our biomimetic conventional outflow tract exhibited in vivo-like characteristics (ultrastructure, cytoskeletal orientation/organization, marker-gene expression, extracellular matrix (ECM) deposition, and outflow regulation). In particular, the biomimetic conventional outflow tract exhibited homeostatic responses to elevated pressure and physiological responses to pharmacotherapies and gene transfer. This model can be used to understand the physiology of the conventional outflow tract and the pathology of glaucoma, as well as to predict the physiological responses of its in vivo counterpart in the development of glaucoma pharmacotherapy. In addition, this modality may also facilitate more rapid development of technologies for glaucoma diagnosis and treatment.
Email: cula.dautriche@downstate.edu