In the second experiment that was done for the paper, whole mounted retinas from control and P23H rats were labeled with Cx43 and GFAP. The results indicated that the density of Cx43 IR puncta in GCL was greater in the P23H rats. Cx43 levels were increased 2 fold in the P23H rat retinas compared to the control. The results suggest that there is a role of Cx43 in the pathogenesis of degeneration. The expression observed in P23H rats correlated with astrocyte hypertrophy suggests an increment of Cx43 expression per astrocyte. Retinal immunofluorescence was done using the marker GFAP and vimentin. Immunofluorescence of GFAP protein was done. P23H rats showed intense GFAP immunoreactivity and revealed colocalization between intermediate filament proteins. The vimentin/GFAP positive Muller cells extended into the subretinal space and expanded, filling areas left by degenerated photoreceptors. There was a 7.8-5.3 fold increase in GFAp expression in the P23H rats compared to the control. This data suggest that the GFAP expression increased in retinal degeneration. The increased GFAP expression is also thought to stabilize newly formed terminal processes of Muller cells and provide resistance to the stress and is essential for the formation of glial scars neurite growth infiltration of monocytes neovascularization, and integration of cells in retinal transplants. GFAP immunoreactivity was analyzed in the ONL of whole mounted retinas from control and P23H rats. In P23H rats, there was more loss of photoreceptors in the ONL which was linked to the appearance of hypertrophied side branches of muller cells into the outermost photo layer. Most of the cone cells also expressed a short morphology. The loss of rod cells also altered the cone mosaic in the ONL there is a correlation between the ring-like area of cone degeneration and the muller cell apical processes. The results suggest that the orientation of the cone cells are disrupted by cone degeneration with muller cell apical processes forming clusters. This also indicates that the loss of photoreceptors induces changes in vascular tissue that activates muller cells. The overall research shows that the disease in the photoreceptor cells also affects the cells that are around those cells, and as a result, there is a need to take into account when discovering future research.
To do the experiments P23H-1 line rat is often used. To a certain extent. It presents a similar phenotype but not the genotype since the mutated rhodopsin protein gene sequence is inserted into the rats and the preexisting normal rhodopsin was not mutated. In addition, the rats that were used in the studies had 18 copies of the mutated gene, whereas in a human there would be one or two at most. It added to the understanding of the disease by creating a model of the disease that can be studied, even though the model is an imperfect one.
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