Polansky J R

Tamm E R, Polansky J R

Lindsey J D, Gaton D D, Sagara T, Polansky J R, Kaufman P L, Weinreb R N

Topical prostaglandin treatment in monkeys reduced TIGR/myocilin protein in the ciliary muscle, suggesting a potential mechanism for prostaglandin-induced uveoscleral outflow increase relevant to glaucoma therapy.

Polansky J R, Fauss D J, Zimmerman C C

This study found that protective factors like bFGF can reduce glucocorticoid-induced TIGR/MYOC expression in human trabecular meshwork cells, while TIGR mutations disrupt protein processing, potentially contributing to glaucoma pathogenesis.

Polansky J R, Nguyen T D

Recent genetic advances, especially the TIGR gene's role in glaucoma, reveal pathogenic mechanisms. This improves diagnosis, understanding disease causes, and developing better treatments for various glaucoma types.

Lütjen-Drecoll E, May C A, Polansky J R, Johnson D H, Bloemendal H, Nguyen T D

This study found stress proteins alpha B-crystallin and TIGR were more widespread and intense in glaucomatous trabecular meshwork. This suggests their involvement in glaucoma's disease process and potential as biomarkers.

Lerner L E, Polansky J R, Howes E L, Stern R

This study found significant hyaluronan in healthy trabecular meshwork endothelial cells, suggesting its crucial role in regulating aqueous outflow resistance and offering a baseline for glaucoma research.

Stone E M, Fingert J H, Alward W L, Nguyen T D, Polansky J R, Sunden S L et al.

Researchers identified a gene (TIGR) on chromosome 1q causing primary open-angle glaucoma. Mutations in TIGR were found in 3.9% of patients, aiding early diagnosis and treatment.

Shirato S, Murphy C G, Bloom E, Franse-Carman L, Maglio M T, Polansky J R et al.

This study characterized phagocytosis in human trabecular meshwork cells, finding a sigmoid-like uptake curve, significant cell changes, and maximum phagocytosis around 96 hours, which is relevant for understanding outflow resistance in glaucoma.

Yun A J, Murphy C G, Polansky J R, Newsome D A, Alvarado J A

HTM cells secrete most ECM proteins, but dexamethasone uniquely induced elastin production. This suggests a mechanism for steroid-induced glaucoma.

Perkins T W, Alvarado J A, Polansky J R, Stilwell L, Maglio M, Juster R

HTM cell monolayers on filters showed hydraulic conductivity mimicking outflow. Cytochalasin B dramatically increased conductivity by cell retraction, offering a model to study aqueous outflow regulation.

Weinreb R N, Polansky J R, Alvarado J A, Mitchell M D

HTM cells metabolize arachidonic acid into diverse eicosanoids (PGE2, PGF2α, HETEs, LTB4), suggesting complex roles in aqueous outflow regulation and potential therapeutic targets.

Shuman M A, Polansky J R, Merkel C, Alvarado J A

Human trabecular meshwork cells produce abundant t-PA, a clot-dissolving enzyme, with minimal inhibitor. This suggests fibrinolysis is crucial for maintaining outflow and preventing glaucoma.

Weinreb R N, Ryder M I, Polansky J R

Studying monkey trabecular cells, researchers found actin filaments are crucial for cell shape and organization, suggesting their importance in outflow regulation relevant to glaucoma.

Weinreb R N, Polansky J R, Kramer S G, Baxter J D

Oral dexamethasone acutely raised IOP in glaucoma patients, especially 4-8 hours post-dose. This suggests glucocorticoids play a significant, rapid role in IOP regulation.

Polansky J R, Wood I S, Maglio M T, Alvarado J A

Cultured human trabecular cells maintain key structural/functional properties, including phagocytosis and ECM production, crucial for understanding outflow pathway health and glaucoma pathology.

Weinreb R N, Mitchell M D, Polansky J R

Human trabecular cells produce prostaglandins, which dexamethasone significantly inhibits. This finding suggests a mechanism for steroid-induced glaucoma by interfering with natural IOP regulation.

Alvarado J A, Wood I, Polansky J R

This study characterized cultured human trabecular cells, finding they retain key features of in-vivo cells, offering a valuable model to understand glaucoma's cellular basis.

Weinreb R N, Bloom E, Baxter J D, Alvarado J, Lan N, O'Donnell J et al.

This study found functional glucocorticoid receptors in human trabecular cells, suggesting direct steroid action on these cells could contribute to steroid-induced glaucoma by impairing aqueous outflow.

Polansky J R, Weinreb R N, Baxter J D, Alvarado J

Researchers successfully grew human trabecular cells in culture using specific conditions, including FGF. This provides a vital tool to study these cells, crucial for understanding glaucoma.