Our laboratory is in the North Texas Eye Research Institute at the University of North Texas Health Science Center. Our laboratory is dedicated to dissecting the molecular mechanisms responsible for glaucomatous trabecular meshwork damage, elevated IOP, as well as damage to the retina, optic nerve, and visual sensing structures in the brain. Our approach utilizes in vitro, in vivo, and ex vivo model systems combined with advanced molecular genetics, physiology, and imaging techniques.
- Glaucomatous damage to TM cells
Elevated IOP is one of the primary risk factors in the development of glaucoma. The trabecular meshwork (TM) is a critical tissue involved in the outflow of aqueous humor and regulation of IOP. Changes in the extracellular matrix (ECM) environment in the TM can alter the ability of aqueous humor to properly drain from the anterior chamber. The involvement of TGF-β2 signaling pathways in the regulation of the ECM in the TM has been extensively studied. Recent evidence has implicated toll-like receptor 4 (TLR4) in the regulation of ECM and fibrogenesis in other tissues such as liver, kidney, lung and skin. Current studies in our laboratory are studying crosstalk between the TGFβ2 signaling pathway and the TLR4 signaling pathway in the regulation of the ECM in the TM. These studies could provide new targets to lower IOP and further explain the mechanisms involved in the development of glaucomatous TM damage.
- RGC death in PCG
Primary congenital glaucoma (PCG) is a severe form of glaucoma with age of onset from birth to 3 years of age. PCG causes high IOP, death/damage to RGCs and the optic nerve, and can lead to permanent loss of vision. The cellular mechanisms leading to RGC loss and optic nerve damage are unknown. Clinical studies have suggested that certain RGC subpopulations are more susceptible to glaucomatous damage. By identifying the pattern and timing of cell death of RGC subtypes, we can elucidate mechanistic pathways that predispose RGCs and their axons to failure and/or death. Recently a mouse model of congenital glaucoma was discovered. Mutation in the Sh3pxd2b gene (referred to as nee) causes anterior segment dysgenesis, elevated IOP, RGC death, and optic nerve damage. Our hypothesis is PCG phenotypes in nee mice cause RGC subtype specific cell death over time. We propose to identify RGC subtype specific cell death utilizing nee mice and substrains of mice with GFP selectively expressed by individual RGC subtypes. This unique study will help identify different susceptibilities in RGC subtypes to PCG induced cell death and help to determine the pattern and mechanism of cell death/damage leading to visual field defects in PCG.
Research Associate: Sherri Harris
Graduate Students: Humberto Hernandez, Steffi Daniel
This page was last modified on May 24, 2016