Millar J Cameron

Roy Chowdhury Uttio, Millar J Cameron, Holman Bradley H, Anderson Kjersten J, Dosa Peter I, Roddy Gavin W et al.

ATP-sensitive potassium channel openers (CKLP1, diazoxide) effectively lowered intraocular pressure in ocular hypertensive mouse models by decreasing episcleral venous pressure, suggesting a new glaucoma treatment approach.

McDowell Colleen M, Kizhatil Krishnakumar, Elliott Michael H, Overby Darryl R, van Batenburg-Sherwood Joseph, Millar J Cameron et al.

This paper provides consensus recommendations for mouse models of ocular hypertension, aiming to standardize research and improve understanding of aqueous humor outflow dysfunction in glaucoma.

Mody Avani A, Millar J Cameron, Clark Abbot F

Studying mice, researchers found that increasing ID1 and ID3 genes blocked TGFβ2-induced high eye pressure and improved fluid outflow, suggesting these genes are potential glaucoma drug targets.

Patel Gaurang C, Millar J Cameron, Clark Abbot F

This study found glucocorticoid receptor transactivation, not transrepression, causes steroid-induced glaucoma. This suggests safer steroid therapies can be developed by targeting transactivation.

Hernandez Humberto, Millar J Cameron, Curry Stacy M, Clark Abbot F, McDowell Colleen M

Studying BAMBI's role in glaucoma, researchers found that reducing BAMBI in the trabecular meshwork increases ECM, reduces outflow, and causes ocular hypertension, highlighting its potential as a therapeutic target.

Webber Hannah C, Bermudez Jaclyn Y, Millar J Cameron, Mao Weiming, Clark Abbot F

Wnt/β-catenin signaling increases K-cadherin in trabecular meshwork, enhancing cell resistance and lowering IOP. This suggests K-cadherin could be a therapeutic target for glaucoma.

Raychaudhuri Urmimala, Millar J Cameron, Clark Abbot F

This study found that increased tissue transglutaminase (TGM2) elevates intraocular pressure in mice by increasing outflow resistance, suggesting TGM2 may contribute to glaucoma.

Roy Chowdhury Uttio, Rinkoski Tommy A, Bahler Cindy K, Millar J Cameron, Bertrand Jacques A, Holman Bradley H et al.

CKLP1, a novel drug, lowers eye pressure by reducing episcleral venous pressure and distal outflow resistance. Its unique mechanism allows additive pressure reduction when combined with existing glaucoma medications, offering new treatment options.

Kasetti Ramesh B, Phan Tien N, Millar J Cameron, Zode Gulab S

Mutant myocilin causes glaucoma by inducing abnormal intracellular accumulation of specific ECM proteins in trabecular meshwork cells, reducing outflow and elevating IOP.

Millar J Cameron, Phan Tien N, Pang Iok-Hou, Clark Abbot F

This study found that in mice, uveoscleral outflow and aqueous humor formation decrease with age, with significant strain-specific differences in these and other aqueous humor dynamics parameters. This provides a foundation for glaucoma research.

Mao Weiming, Millar J Cameron, Wang Wan-Heng, Silverman Sean M, Liu Yang, Wordinger Robert J et al.

This study confirmed a functional canonical Wnt pathway in the human trabecular meshwork. This pathway, not non-canonical Wnt signaling, regulates intraocular pressure, suggesting a potential therapeutic target for glaucoma.

Millar J Cameron, Clark Abbot F, Pang Iok-Hou

This study developed a mouse model to precisely measure all aqueous humor dynamics, showing common glaucoma drugs act via distinct mechanisms, which is crucial for evaluating new therapies.

Shepard Allan R, Millar J Cameron, Pang Iok-Hou, Jacobson Nasreen, Wang Wan-Heng, Clark Abbot F

Active TGFbeta2 gene transfer in rodents elevated intraocular pressure and reduced outflow facility, creating a glaucoma model to study disease mechanisms and potential therapies.

Wang Wan-Heng, Millar J Cameron, Pang Iok-Hou, Wax Martin B, Clark Abbot F

A rebound tonometer accurately measured intraocular pressure in rats and mice, providing a valuable non-invasive tool for glaucoma research and understanding its etiology and pathology.