The finding also reveals how the retina's own stem cells can be directed to aid the growth of new cells to replace diseased or dying ones in the eye. Study results appear in the June 24 issue of the journal Science.
Anne L. Calof in the Department of Anatomy and Neurobiology and her UCI colleagues have identified how a protein called GDF11 controls a key component of retinal-cell differentiation during development, which makes GDDF11 an attractive therapeutic target.
"By manipulating the ability of this protein to control cell development, there is the potential for therapeutics to harness the power of the stem cells that already exist in the retina to replace any retinal cells that have been lost or injured," Calof said. "If so, we thereby may be able to cure visual disorders that result from loss of certain retinal cell types."
During the process of embryonic development, groups of neural precursor cells, which are formed from stem cells, are given brief periods of time to differentiate into their specific tissue forms, a process that is tightly regulated by signaling proteins.
In tests on developing mice, the Calof group observed that the GDF11 protein precisely controls the "window of opportunity" in which retinal precursor cells differentiate into the cells that give rise to the optic nerve. This regulation is important, Calof said, because it assures proper development of the entire retina, a nerve cell layer that lines the back of the eye, senses light and creates the electrical impulses that travel through the optic nerve to the brain.