• Publications
  • Influence
Identification of a Gene That Causes Primary Open Angle Glaucoma
A gene encoding a trabecular meshwork protein (TIGR) mapped to the narrowest disease interval by STS content and radiation hybrid mapping and will aid in early diagnosis of glaucoma.
Inherited glaucoma in DBA/2J mice: pertinent disease features for studying the neurodegeneration.
The period when mice have elevated intraocular pressure extends from 6 months to 16 months, with 8-9 months representing an important transition to high IOP for many mice, and optic nerve degeneration follows IOP elevation, with the majority of optic nerves being severely damaged by 12 months of age.
Characterization of a transformed rat retinal ganglion cell line.
Molecular clustering identifies complement and endothelin induction as early events in a mouse model of glaucoma.
Early-stage expression changes included upregulation of both the complement cascade and the endothelin system, and so the therapeutic value of separately inhibiting them was tested and mice with a mutation in complement component 1a were protected from glaucoma.
TGFbeta2-induced changes in human trabecular meshwork: implications for intraocular pressure.
Investigation of effects of TGFbeta2 on secretion of fibronectin and the protease inhibitor plasminogen activator inhibitor (PAI)-1 from human TM cell cultures and perfused human ocular anterior segments found modulation of T GFbeta2-induced changes in the ECM may provide a novel and viable approach to the management of glaucoma.
Radiation treatment inhibits monocyte entry into the optic nerve head and prevents neuronal damage in a mouse model of glaucoma.
It is shown that the leukocyte transendothelial migration pathway is activated in the optic nerve head at the earliest stages of disease in an inherited mouse model of glaucoma, resulting in proinflammatory monocytes entering the optic nerves prior to detectable neuronal damage.
Non-secretion of mutant proteins of the glaucoma gene myocilin in cultured trabecular meshwork cells and in aqueous humor.
These studies suggest that MYOC glaucoma is due either to insufficient levels of secreted myocilin or to compromised TM cell function caused by congestion of the TM secretory pathway.
Reduction of ER stress via a chemical chaperone prevents disease phenotypes in a mouse model of primary open angle glaucoma.
Reduction of ER stress with a chemical chaperone, phenylbutyric acid (PBA), prevented glaucoma phenotypes in Tg-MYOC(Y437H) mice by promoting the secretion of mutant myocilin in the aqueous humor and by decreasing intracellular accumulation of myociles in the ER, thus preventing TM cell death.
Glucocorticoid-induced formation of cross-linked actin networks in cultured human trabecular meshwork cells.
The steroid-induced alteration in trabecular meshwork cytoskeleton may be an important factor in the development of steroid- induced ocular hypertension and may play a role in the ocular pulmonary hypertension associated with primary open angle glaucoma.