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Enhanced FGF-2 movement through human sclera after exposure to latanoprost
M Aihara1, J D Lindsey, R N Weinreb
1Glaucoma Center, University of California San Diego, La Jolla 92093-0946, USA.
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.