Purpose: To modulate optic nerve regeneration by reducing the inhibitory effects of reactive astrocytes.
Methods: Bcl-2 over-expression transgenic mice were mated with GFAP/Vimentin double gene knock out mice (GFAP-/-/Vim-/-) to produce Bcl-2 tg/GFAP-/-/Vim-/- triple mutant mice (3M). Optic nerve crush model was established respectively in 3 P5 and 3 P18 mice. GAP43 immunofluore-scence was used to specifically label regenerative axons.
Results: Optic nerve regeneration was observed in P5 3M mice all the way to optic chiasm in P18 3M mice, only local sprouting regeneration was observed.
Conclusions: With reestablishment of intrinsic ability of retinal ganglion cells by Bcl-2 transgenic, optic nerve regeneration is promoted by reducing the inhibitory effects of reactive astrocytes, which demonstrates reactive astrocyte as an important factor inhibiting optic regeneration and provides new direction for regenerative therapy in glaucoma.