Retinal neovascularization induced by mutant gene inhibited in an inherited retinitis pigmentosa mouse model: an study.

AIM

To explore whether the retinal neovascularization (NV) in a genetic mutant mice model could be ameliorated in an inherited retinitis pigmentosa (RP) mouse, which would help to elucidate the possible mechanism and prevention of retinal NV diseases in clinic.

METHODS

The mice, the genetic mutant mouse model of retinal NV caused by the homozygous mutation of gene, with the mice, the inherited RP mouse caused by homozygous mutation of gene were bred. Intercrossing of the above two mice led to the birth of the F1 hybrids, further inbreeding of which gave birth to the F2 offspring. The ocular genotypes and phenotypes of the mice from all generations were examined, with the F2 offspring grouped according to the genotypes.

RESULTS

The mice exhibited the RP phenotype of outer retinal degeneration and loss of retinal function. The mice exhibited the phenotype of retinal NV obviously shown by the fundus fluorescein angiography. The F1 hydrides, with the heterozygote genotype, exhibited no phenotypes of RP or retinal NV. The F2 offspring with homozygous genotypes were grouped into four subgroups. They were the F2-I mice with the wild-type and genes ( - ), which had normal ocular phenotypes; the F2-II mice with homozygous mutant gene ( - ), which exhibited the retinal NV phenotype; the F2-III mice with homozygous mutant gene ( - ), which exhibited the RP phenotype. Specifically, the F2-IV mice with homozygous mutant and gene ( - ) showed only the RP phenotype, without the signs of retinal NV.

CONCLUSION

The retinal NV can be inhibited by the RP phenotype, which implies the role of a hyperoxic state in treating retinal NV diseases.