Lindsey J D

Leung C K S, Lindsey J D, Chen L, Liu Q, Weinreb R N

This study found severe retinal ischemia causes early, non-progressive RGC loss, detectable by blue-light imaging. Milder ischemia caused no significant loss. This highlights the timing and severity of RGC damage.

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.

Schachtschabel U, Lindsey J D, Weinreb R N

Prostaglandins lower eye pressure by activating ciliary muscle receptors, leading to matrix metalloproteinase production. These enzymes remodel ciliary muscle, increasing uveoscleral outflow, clinically relevant for glaucoma treatment.

Gaton D D, Sagara T, Lindsey J D, Weinreb R N

MMP-1 was found prominently in normal human uveoscleral outflow tissues, especially ciliary muscle. This suggests MMP-1 activity helps regulate uveoscleral outflow, impacting intraocular pressure control.

Liu J H, Lindsey J D, Weinreb R N

Rabbit aqueous humor protein concentration has an endogenous circadian rhythm affecting major proteins, independent of sympathetic nerves. This clarifies ocular fluid dynamics.

Lindsey J D, Kashiwagi K, Kashiwagi F, Weinreb R N

This study found prostaglandins increase ciliary muscle extracellular matrix turnover, likely explaining how these glaucoma drugs enhance uveoscleral outflow and reduce eye pressure.

Lindsey J D, Weinreb R N

Researchers developed a defined system to study purified rat retinal ganglion cells (RGCs). They found hydrocortisone and progesterone enhanced RGC survival, providing a tool for understanding RGC regulation relevant to glaucoma.

Weinreb R N, Lindsey J D, Sample P