Enhanced FGF-2 movement through human sclera after exposure to latanoprost

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 ve hicle for 3 days. Transscleral permeability was then assessed by placing ea ch 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. Tr ansscleral permeation by 10-kDa tetramethylrhodamine-dextran also was deter mined, for comparison. RESULTS. Transscleral permeation by FGF-2 through sclera that had been incu bated with vehicle was 1.53 +/- 0.86 x 10(-8) cm/sec. Transscleral permeati on 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 aci d was increased by an average of 48% +/- 62%, 100% +/- 108%, and 108% +/- 7 9%, 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 n M 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 refl ect a general enhancement of permeability, a possibility that future in viv o studies should explore.