To answer the question about whether or not NPD1 could prevent cell death caused by an excess of A2E known to accumulate in the RPE during aging and to be exaggerated in age-related macular degeneration, the researchers added NPD1 to an A2E-induced experimental model and found it not only stopped programmed cell death, but that the protective effects were present even six hours later. The team decided to explore whether oxidative stress triggered by another experimental condition, called serum starvation/H2O2/TNF,, would be similarly inhibited. NPD1 also exerted protection in this experimental condition. Addition of NPD1 even eight hours after triggering oxidative stress resulted in protection. In a series of further experiments to delineate how NPD1 acts, the scientists found that NPD1 elicits a specific action rather than antioxidant activity to counteract A2E-induced cell death in RPE cells.
One of these papers reports also the discovery that the daily interaction of photoreceptors and RPE cells balance against damage is maintained by NPD1.
The regulation of these proteins involved in cell survival or death shown by this research will help us define NPD1 survival bioactivity in the RPE cell, notes Dr. Bazan. These events are clinically significant because they may allow the exploration of therapeutic interventions for retinal degenerative diseases such retinitis pigmentosa.