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Wenjie Hu, Liwei Zhang, Zhongshu Tang; Caveolin-1 Protects retinal ganglion cells(RGCs) in a Glaucoma Model. Invest. Ophthalmol. Vis. Sci. 2018;59(9):6121.
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© ARVO (1962-2015); The Authors (2016-present)
Glaucoma is a group of irreversible eye diseases. Of its popular features, RGCs death is the principal as some others are actually parts of RGCs degeneration: optic nerve atrophy is the defect of RGC axons and visual field loss is the failure of RGCs function. Accordingly, RGCs protection is essential in glaucoma treatment. Here we report that Caveolin-1 (Cav1), a factor reported in a GWAS to be associated with glaucoma, protects RGCs in an acute ocular hypertension model.
In this study, Wild-type (C57BL/6J) mice and Cav1 KO mice under normal and acute ocular hypertension condition were used to analysis the function of Cav1. Cav1 expression was detected by immunofluorescent staining and western blot. TUNEL staining and Fluoro-Gold (FG) retrogradely labeling RGCs, were used to study RGCs apoptosis and survival in retina respectively. We use Q-PCR and immunofluorescent staining to understand the number and distribution of microglia.
Cav1 expression was upregulated in the model. RGCs survival was enhanced by the application of cavtratin, a membrane permeable peptide containing the Cav1 scaffolding domain. On the other hand, Cav1 deficiency enhanced apoptosis throughout retina. We further found that cavtratin reduced microglia number and altered their distribution. It also promoted the transition of microglia from M1 to M2 state, which suggests that Cav1 achieved its neuroprotection by regulate the number, distribution and state of retina microglia.
Taken together, our data highlights the neuroprotective role of Cav1 in the acute ocular hypertension injury and provide a novel therapeutic target for glaucoma.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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