Intensive light exposure inducing choroidal neovascularization in TgAPPswe/PS1 transgenic mice
10.13389/j.cnki.rao.2017.0027
- VernacularTitle:高强度光照损伤致TgAPPswePS1转基因鼠脉络膜新生血管形成
- Author:
Zhizhang DONG
;
Juan LI
;
Xuerong SUN
;
Jian GE
- Keywords:
light injury;
transgenic mouse;
choroidal neovascularization;
age-related macular degeneration
- From:
Recent Advances in Ophthalmology
2017;37(2):101-105
- CountryChina
- Language:Chinese
-
Abstract:
Objective To research the choroidal neovascularization (CNV)in TgAPPswePS1 transgenic mice after intensive light exposure injury.Methods Twenty TgAPPswe/PS1 transgenic mice at the age of 6 months were grouped for experiments.The treated groups of 12 mice were treated by a source of 10 000 lux cool full spectrum light for 6 months,12 hours per day;While the control groups of 8 mice were kept in normal conditions.The mice eyes of the experimental group and control group were examined with HE/Toluidin blue staining,the retinal structure was observed,and the number of CNV was counted.The expression of VEGF and Aβ were examined with immunofluorescence on the retinal pigment epithelial (RPE) flat mount.All of the results were quantified and statistically analyzed.Results After treated by 6 months of intensive light exposure in the experimental group,histopathological analysis has found significant loss of outer nuclear layer/photoreceptor out segment and outer plexiform layer as compared with the control group;At the same time,abnormal hypo-and hyper-pigmentation,vacuoles and disruption in the RPE layer,remarkable CNV were found in the experiment group by Toluidin blue staining,and the incidence of CNV was 18.75％.The VEGF expression domenstrated.a diffusive and deposition pattern along the neovessels which showed a significant increase of (6.59 ± 1.14) fold changes as compared with the control group.The difference was statistical significant (P ＜ 0.05).Then the Aβ deposits were positive expressed in the RPE layers after intensive light exposure treatment,and pathological deposition of Aβ in the RPE showed plaque like displayed by confocal Z-stack microscopy,and the drusenoid Aβ deposits were found alone with the neovessels on the RPE flat mount.The deposition of Aβ protein increased with (6.45 ± 2.93) fold changes as compared with the control group,and the difference was statistical significant.Conclusion CNV with degenerative changes in the outer retina can be induced by intensive light exposure in the APPswe/PS1 transgenic mouse.These results suggest that an Alzheimer's transgenic animal model might be an alternative animal model for CNV if combined with intensive light exposure.
