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Makoto Aihara, James D. Lindsey, Robert N. Weinreb; Enhanced FGF-2 Movement through Human Sclera after Exposure to Latanoprost. Invest. Ophthalmol. Vis. Sci. 2001;42(11):2554-2559. doi: https://doi.org/.
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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 × 10−8 cm/sec.
Transscleral permeation by 10-kDa tetramethylrhodamine-dextran was
1.04 ± 0.39 × 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
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