Washington: Scientists at Schepens Eye Research Institute have found that cells in the retina known as glial cells, set up a physical barrier that prevents retinal transplants from migrating, growing and hooking up to the host retina and the optic nerve to restore sight.

They have also found that disarming these cells can free transplanted tissue to make the sight-saving connection to the retina and the optic nerve and ultimately to the brain. These findings are published in the August issue of 'Nature Neuroscience'.

The retina is the paper-thin, light-sensitive tissue at the back of the eye that takes light and images from the outside world and transmits them through the optic nerve to the brain. Retinal cells that sense the light and send the information to the brain are nerve cells.

Glial cells, which are support cells to nerve cells, are found in all nerve tissue, such as the brain, the spinal cord and the retina. In injured or diseased eyes, glial cells cause the increase of certain proteins called intermediate filament proteins. These proteins help the glial cells to form a scar around the injured or damaged area and appear to be essential to the development of these scars.

To test this theory, Dong Feng Chen, assistant scientist at Schepens Eye Research Institute and his research team injected retinal cells from "green mice", (cells of these mice carry a green fluorescence gene and reveal green colour so their transplanted tissue can be detected easily in non-green mice) into mice with normal glial cells and also into mice whose glial cells had been manipulated so that the scar-forming proteins were missing or "knocked out".

In the mice with normal glial cells, Chen and her colleagues found that the transplanted green cells remained near the injection site, did not grow or migrate to other area of the retina, and did not grow the nerve tentacles necessary to wire up to the host retinas and the optic nerve. The team also found that the glial cells surrounded the transplanted tissue, formed a scar, a physical barrier that kept the transplanted tissue from integrating into the eye and connecting to the optic nerve.

In contrast, when Chen's team looked at the knockout mice in which the scar-forming proteins were missing, the transplanted green cells had survived, migrated to the retina, grew the necessary tentacles and became entwined in the optic nerve. Divested of the filament proteins, the glial cells did not form a physical scar barrier.

Chen says that this discovery greatly increases the chances that retinal transplants may some day be able to survive in the human eye. And, since glial cells are in other parts of the nervous tissues, their manipulation may lead the way to the survival of other types of neural transplantations, such as those being attempted for Parkinson's disease.

Chen also feels that these findings will ultimately impact the success of retinal transplantation and restore vision to millions afflicted by retinal diseases such as macular degeneration, glaucoma, and retinitis pigmentosa.

ANI