Abstract
Non-exudative age-related macular degeneration (AMD) is an irreversibly progressive retinal degenerative disease characterized by dysfunction and loss of retinal pigment epithelium (RPE). It has been suggested that impaired phagocytosis of the RPE is involved in the progression of non-exudative AMD, but the mechanism is not fully clear. In this study, we investigated the effect of lipid droplet accumulation on RPE function. Compared to young mice, the expression of lipid droplet-associated proteins increased in the RPE-choroidal complex, and lipid droplet in the RPE was observed in aged pigmented mice (12-month-old). Repeated treatment of the photoreceptor outer segment against ARPE-19 resulted in lipid droplets in ARPE-19 cells in vitro. Oleic acid treatment for ARPE-19 cells to form intracellular lipid droplet reduced the POS uptake into the ARPE-19 cells without causing a decrease in cell viability. The suppression of the POS uptake by lipid droplet formation improved by inhibiting lipid droplet formation using triacsin C. Moreover, the amount of intracellular reactive oxygen species was suppressed by the triacsin C treatment. These results indicate that lipid droplet is involved in the RPE dysfunction, and inhibiting lipid droplet formation may be a target for preventing and treating non-exudative AMD.
Highlights
Photoreceptor cells are essential for light reception and vision maintenance, and they receive nutritional and functional support from retinal pigment epithelium (RPE)cells
We compared adipose differentiation-related protein (ADRP) and tail-interacting 47 kDa protein (TIP47), which are localized on the lipid droplet membrane [18], in the neural retina and RPEchoroid complex of young and aged mice
Lipid droplet were not observed in the RPE of young mice; they were observed in the RPE of aged mice (Figure 1C)
Summary
Photoreceptor cells are essential for light reception and vision maintenance, and they receive nutritional and functional support from retinal pigment epithelium (RPE). The non-exudative age-related macular degeneration (AMD) is a disease in which the central lesion is atrophy and loss of function of the RPE. In early AMD, lipofuscin and lipid-derived components called drusen accumulate inner or outer of the RPE cells due to dysfunction of the RPE [3,4]. Chronic accumulation of them is believed to cause cell death and geographic atrophy of RPE cells, leading to subsequent photoreceptor cell death [5,6,7]. The progression of non-exudative AMD is considered irreversible, and it is essential to intervene as early as possible. It has been reported that autophagy failure of the RPE is involved in the development and progression of non-exudative AMD [3,4]
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