Compared to birds, the scientist said, mammals have an even more limited Mller glia cell response to injury. In an injured mouse or rat retina, the cells may react and become larger, but few start dividing again.
Because the Mller glia cells appeared to have the potential to regrow but won't do so spontaneously after an injury, several groups of researchers have tried to stimulate them to grow in lab dishes and in lab animals by injecting cell growth factors or factors that re-activate certain genes that were silenced after embryonic development. These studies showed that the Mller glia cells could be artificially stimulated to start dividing again, and some began to show light-detecting receptors. However, these studies, the researchers noted, weren't able to detect any regenerated inner retina nerve cells, except when the Mller glia cells were genetically modified with genes that specifically promote the formation of amacrine cells, which act as intermediaries in transmitting nerve signals.
"This was puzzling," Reh said, "because in chicks amacrine cells are the primary retinal cells that are regenerated after injury." To resolve the discrepancy between what was detected in chicks and not detected in rodents, the Reh laboratory conducted a systematic analysis of the response to injury in the mouse retina, and the effects of specific growth factor stimulation on the proliferation of Mller glia cells.
The researchers injected a substance into the retina to eliminate ganglion cells (a type of nerve cell found near the surface of the retina) and amacrine cells. Then by injecting the eye with epidermal growth factor (EGF), fibroblast growth factor 1 (FGF1) or a combination of FGF1 and insulin, they were able to stimulate the Mller glia cells to re-start their dividing engines and begin to proliferate across the retina.
The proliferating Mlle
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University of Washington