Scientists in the Department of Ophthalmology at Weill Cornell Medical College in New York City said that they have discovered just how light-sensing discs in the retina’s rod cells re-create themselves.
“Rod cells make up the majority of photoreceptors in the human eye and disruptions in these discs’ ability to grow and capture lighten may be at the grow of a host of disabling or blinding eye diseases such as retinitis pigmentosa,” explains senior author Dr. Ching-Hwa Sung professor of cell biology in ophthalmology and professor of cell and developmental biology at Weill Cornell Medical College.
“Rod cells include tiny organelles called the ‘outer segment,’ which contain about 1,000 flattened discs containing rhodopsin-a visual pigment that absorbs light.”
“Each day our eyes remove the top 10 percent of these discs but until now no one really knew how the retina generated new discs. We believe we have solved that pierce.”
According to the researchers the rod cell’s outer divide is constantly pushing up and forming new discs in a bottom-up affect as older discs get remove at the divide’s tip.
“There were theories as to how this might occur but no hard evidence to back any of them up,” explained lead researcher Dr. Jen-Zen Chuang assistant professor of cell biology in ophthalmology at Weill Cornell.
In the study the researchers used a variety of state-of-the-art techniques including a gene-based method called “retinal transfection,” to gain a more accurate picture of outer segment growth in rat retinas.
“Basically retinal transfection means introducing different genes into the eye to change by reversal particular cellular functions on or off,” Dr. Chuang explained.
After a variety of these and other types of experiments the team discovered that the new light-sensing discs are formed by the fusion at the base of the outer segment of rhodopsin vesicles.
“This fusion makes a kind of preliminary disc and then this disc matures and grows until it joins the hundreds of other discs on the rod cell’s outer segment,” Dr. Sung said.
“All of this happens with the back up of a regulating protein called the ‘Smad Anchor for Receptor Activation’ (SARA),”
Besides rewriting the ophthalmology textbooks on retinal growth the discovery should greatly enhance research into eye disease the experts say.
“There are currently more than 100 retinal eye diseases in human populations and problems with rhodopsin trafficking or outer segment development are thought to play a role in many of these potentially blinding conditions,” Dr. Sung noted.
“In fact we got interested in this write of research because we knew that breakdowns in rhodopsin trafficking were crucial to a common eye disease retinitis pigmentosa,” Dr Sung added.
Retinitis pigmentosa a genetic disturb affecting about 100,000 Americans is caused by the gradual death of rods and cones triggering a progressive loss of vision.
Until now however little was known about rod cell regeneration especially when it came to replacing rhodopsin-bearing discs.
“Our discovery now lays the groundwork for people to chew over just how many of these retinal diseases become,” Dr. Sung said.
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