uf-021 and Corneal-Diseases

Deleterious effects of isopropyl unoprostone (PG-F2 alpha) on the ocular surface were evaluated using the in vivo barrier function assay of corneal epithelial cells and the proliferation assay of human corneal epithelial cells in vitro. The barrier function of corneal epithelial cells in vivo was not impaired by treatment with PGF2 alpha, but it was significantly suppressed by timolol. The result of cell proliferation assay of human corneal cells showed that the 0.12% PGF2 alpha ophthalmic solution caused greater suppression of cell proliferation and acuter cell toxicity than 0.5% timolol ophthalmic solution. Further study showed that not the vehicle but the PGF2 alpha itself was responsible for these deleterious effects. We conclude that the 0.12% PGF2 alpha ophthalmic solution affects cell migration and proliferation but not the barrier effects of the ocular surface. These results suggest that the corneal epithelial defect of glaucoma patients may be caused by these two independent mechanisms, namely suppression of cell proliferation by PGF2 alpha and the destruction of the barrier function of the ocular surface by timolol.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Cell Division; Cells, Cultured; Corneal Diseases; Dinoprost; Epithelium, Corneal; Female; Humans; Male; Middle Aged; Ophthalmic Solutions; Timolol