Retinal pigment epithelium cell-derived microparticles mediate oxidative stress-induced retinal cells dysfunction

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Age-related macular degeneration (AMD) represents the leading cause of vision loss in the elderly. The cumulative oxidative injury induces retinal pigment epithelium (RPE) membrane microparticles production, RPE cell death and cellular senescence. The RPE blebs are implicated in the formation of sub-retinal deposit. Nonetheless, the pathophysiological roles of RPE microparticles (RMPs) remain largely unexplored. This study was designed to investigate whether RMPs participate in the retinal cells dysfunction.


RMPs and fluorescent DiI-labelled RMPs were isolated from cultured ARPE-19 cells under oxidative stress. RMPs-treated RPE cells were subjected to WST-1, cellular senescent, apoptotic assay and FACS cell cycle analysis respectively. The antibody against CD36 was used in uptake experiment to determine the involvement of scavenger receptor CD36.


Our study revealed that uptake of RMPs by RPE cells is time-dependent, and this process is partially dependent on CD36 evidenced by an approximately 50% decrease of RMPs uptake caused by CD36 antibody treatment. In addition, RMPs significantly reduced RPE cell viability in a dose-dependent manner. RMPs in a concentration of 5% μg/ml significantly induced RPE cell-cycle arrest at G0/G1 phase. RMPs-treated cells exhibited a 19% increase in G0/G1 phase, with associated increases of the senescence-associated β-galactosidase activity.


We demonstrated for the first time that RPE cells uptake microparticles derived from RPE cells under oxidative stress. These findings strongly suggest that RMPs function as mediators to exacerbate the oxidative damages to RPE cells, and indicate a pathological role of RMPs in AMD.

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