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Damaging Healthy Eye Cells: New Insights Into Diseases Causing The Loss Of Vision.

There are two major light in the mammalian eye: . New research by scientists from have shown that dying can trigger the demise of healthy , leading to the loss of vision.

The study by and colleagues, published in the journal PLOS Genetics, showed that when a multifunctional protein known as ‘Ran-binding protein 2′ (RanBP2) is removed from cone cells it causes not only those cells to die but also results in the demise of the healthy rod cells in the eye. The authors also show that the rod and cone cells undergo a cascade of distinct and unusual events as they are dying. The demise of these cells can play a part in diseases such as retinitis pigmentosa and age-related macular degeneration (AMD).

The opposite case – that dying rod cells can trigger the demise of healthy cone cells – has long been known. This rod-triggered cell death results in a gradual but ultimately complete loss of human vision, because cone cells are essential for seeing in daylight, high acuity and colour vision (whereas rods help vision in low-light environments and peripheral vision). The cone-triggered cell death demonstrated by Kyoung-in Cho and colleagues is the first time that this has been shown to happen the other way.

These results have critical implications for understanding common diseases, such as AMD. AMD affects the central region of the human retina (the macula), which is an area that is critical to focused vision (the kind required for reading, driving etc).

As we begin to understand the events causing the death of healthy rods by damaged cones, which may be instrumental in other diseases, hope is raised for new treatments of neurodegenerative diseases affecting these photoreceptors in the eye.

Source

“Distinct and Atypical Intrinsic and Extrinsic Cell Death Pathways between Photoreceptor Cell Types upon Specific Ablation of Ranbp2 in Cone Photoreceptors”,
Cho K-i, Haque M, Wang J, Yu M, Hao Y, et al. (2013)
PLoS Genet. 9(6): e1003555. doi:10.1371/journal.pgen.1003555