FIG. 7.

Cone preservation in the transduced areas of Gucy2e^–/– treated eyes. Shown are adjoining retinal sections of Gucy2e^–/– eyes 6 months post treatment with low-titer vector (a and b) and untreated contralateral eyes (c and d) stained with antibodies against GC1 (a and c, green) and cone α-transducin (b and d, yellow). (e–l) Insets are images of corresponding regions outlined in (a) and (b). In the areas where GC1 staining is evident in the treated eyes (e and g) there is also expression of cone α-transducin (f and h). In the untransduced areas, where there is no GC1 (i and k), there is no cone α-transducin staining (j and l). (m and n) Images of the superior retina, and (o and p) of the inferior retina of the untreated eye (c and d). There is no GC1 staining in the untreated eye (c). Weak cone α-transducin staining is evident in the superior untreated retina (n) with few cone cells present in the inferior part of the retina (p). Scale bars: (a) 500 μm; (e) 100 μm. (r) Number of cone cells determined by cone α-transducin staining in Gucy2e^–/– eyes treated with low-titer vector, compared with untreated Gucy2e^–/– eyes and C57BL/6J wild-type controls. The cone number in treated eyes was 20% higher than in untreated eyes (p<0.001, one-way ANOVA). (s) Real-time RT-PCR quantification of cone arrestin mRNA (CAR) in wild-type, Gucy2e^–/– untreated eyes and eyes 5 months post treatment with high-titer vector. The levels of cone arrestin are 1.3 times higher in treated eyes compared with untreated eyes (p<0.0001, one-way ANOVA) and have increased to 70% of the levels in wild-type eyes. Color images available online at www.liebertonline.com/hum