Parkin is an interesting protein. Encoded in humans by the PARK2 gene, it is implicated in several disease states, including Parkinson’s disease. How PARK2 mutations lead to dopaminergic cell death and early Parkinsonian symptoms isn’t clear, though – it appears to play a role in the degradation of free-radical-damaged mitochondria, but what’s now clear is that parkin also plays a central role in keeping the lens… clear.
Intrigued by the protein’s potential role in lens opacity, researchers from the Charles E Schmidt College of Medicine at Florida Atlantic University decided to delve deeper. They performed cell culture experiments in which lens epithelial cells (LECs) expressing either normal or mutated forms of the PARK2 gene were assessed. What they found was this: PARK2 is expressed when LECs are exposed to cataract-causing, free radical-generating environmental insults (in this case, oxidative stress caused by hydrogen peroxide exposure). Parkin removes damaged mitochondria (see Figure 1), and by doing so, helps prevent the formation of free radicals in LECs. This increases the ability of the LECs to survive free radical formation, and presumably, the reactive oxygen species-mediated aging.
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