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Enhanced FGF-2 Movement through Human Sclera after Exposure to Latanoprost

From the Glaucoma Center, University of California San Diego, La Jolla.

PURPOSE. To determine whether exposure of sclera to latanoprost acid alters transscleral permeation by FGF-2.

METHODS. Pieces of human sclera were isolated from donor eyes after death, placed in organ culture, and exposed to 50 to 200 nM latanoprost acid or vehicle for 3 days. Transscleral permeability was then assessed by placing each scleral piece into a Ussing apparatus and measuring the amount of FGF-2 that moves from the orbital side to the uveal side of the scleral piece. Transscleral permeation by 10-kDa tetramethylrhodamine-dextran also was determined, for comparison.

RESULTS. Transscleral permeation by FGF-2 through sclera that had been incubated with vehicle was 1.53 ± 0.86 x 10^-8 cm/sec. Transscleral permeation by 10-kDa tetramethylrhodamine-dextran was 1.04 ± 0.39 x 10^-6 cm/sec. FGF-2 permeation of sclera exposed to 50, 100, and 200 nM latanoprost acid was increased by an average of 48% ± 62%, 100% ± 108%, and 108% ± 79%, respectively, compared with sclera exposed to vehicle (n = 13; P < 0.05). Scleral permeation by 10-kDa dextran after exposure to 50, 100, or 200 nM latanoprost acid was significantly increased by 42% ± 36%, 59% ± 51%, and 65% ± 49%, respectively (n = 14; P < 0.05). The ratio of dextran to FGF-2 permeation was approximately 90 and did not vary with 50, 100, or 200 nM latanoprost acid (P = 0.93, ANOVA).

CONCLUSIONS. Exposure of sclera to latanoprost acid increases transscleral permeation by FGF-2 in human scleral organ cultures. Because this increase parallels the increased scleral permeability caused by dextran, it may reflect a general enhancement of permeability, a possibility that future in vivo studies should explore.

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