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Abstract
PURPOSE: The aim of this study was to identify whether abnormalities in the synthesis of basic fibroblast growth factor (bFGF) or its receptor (bFGF-R) were responsible for the photoreceptor dystrophy in Royal College of Surgeons (RCS) rats. METHODS: The polymerase chain reaction was used to detect the expression of bFGF and bFGF-R messenger RNA in the retinal pigment epithelial (RPE) cells and the neural retina of RCS dystrophic rats and in PVG/C and RCS-rdy+ control animals. RESULTS: In the RPE, it was found that there was no significant difference in the expression of bFGF and bFGF-R between RCS rats and the controls at the ages of 21 days and 3 mo. In the neural retina, the level of bFGF expression was lower in the 21-day-old RCS rats compared with the control group, but bFGF-R expression was as strong as in the PVG/C and RCS-rdy+ animals. However, in 3-mo-old RCS rat neural retina, the bFGF and bFGF-R expression was found to be significantly lower than in the control animals. CONCLUSIONS: Although the mutant gene in RCS rats is expressed in the RPE cells, these results suggest that there is no significant defect in bFGF or bFGF-R expression in the RPE cells of RCS rats, which would be an initiating factor in the development of photoreceptor degeneration in these animals. The lowered bFGF levels in the neural retina at early stages (postnatal day 21) may explain the prolongation of photoreceptor survival when exogenous bFGF is injected.