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Publication : Neovascularization of the RPE: temporal differences in mice with rod photoreceptor gene defects.

First Author  Nishikawa S Year  1998
Journal  Exp Eye Res Volume  67
Issue  5 Pages  509-15
PubMed ID  9878212 Mgi Jnum  J:52112
Mgi Id  MGI:1328463 Doi  10.1006/exer.1998.0538
Citation  Nishikawa S, et al. (1998) Neovascularization of the RPE: temporal differences in mice with rod photoreceptor gene defects. Exp Eye Res 67(5):509-15
abstractText  Neovascularization (NV) of the retinal pigment epitheium (RPE) by retinal. Capillaries following degeneration and loss of photoreceptor cells is a widely recognized phenomenon in rodents. NV of the RPE usually occurs several weeks to months after the loss of photoreceptor cells. We have observed that Mi of the RPE occurs much earlier in a line of P23H mutant rhodopsin transgenic mice than in most other mice and rats that have been previously examined. To compare the temporal course of RPE NV in P23H mice with that of two other retinal degeneration mutants with the same time course of photoreceptor cell loss, we have quantified the number of retinal capillaries in the RPE of P23H and Q344ter mutant rhodopsin transgenic mice and retinal degeneration (rd/rd) mice at ages ranging from postnatal day (P) 20-400. Retinal capillary profiles located within the RPE were already present as early as P20 in the P23H retinas, and although these usually were located where most photoreceptor nuclei were missing, they occasionally were found where 1-2 rows of photoreceptor nuclei were still present. The maximal incidence was found in P23H retinas at P100. By contrast, NV of the RPE in rd/rd and Q344ter mice occurred much later. In rd/rd, a significant number of capillary profiles was not seen in the RPE until about P130, and not until about P180 in Q344ter. Both showed maximal incidence at about P240. In all three mutants, an apparent regression of the capillaries occurred following the peak, with that in the P23H mice preceeding the other two mutants. The findings suggest that the P23H mutant rhodopsin transgenic mouse may be a useful model for studying the regulation of NV in the outer retina. (C) 1998 Academic Press.
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