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S.T. Beug, G.D. Dakubo, A.P. McMahon, V.A. Wallace; Sonic Hedgehog From Retinal Ganglion Cells Regulates Gliogenesis in the Mammalian Optic Nerve . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3126.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Glial cell development in the mammalian optic nerve depends on retinal ganglion cell (RGC) axons, but the signals that mediate this neuron–to–glial interaction in the optic nerve have not been fully characterized. The morphogen Sonic hedgehog (Shh) is expressed in RGCs and we showed previously that Shh is required for the specification of astrocyte lineage cells at both the optic disc and nerve. Methods: To study the role of RGC–derived Shh at later stages of astrocyte development, we generated mice with a conditional ablation of Shh in the peripheral retina and analyzed gene expression and glial cell development in the optic nerve. Results: Astrocyte development is initiated in these mutant mice; however, the expression of Hedgehog (Hh) target and cell cycle genes in the perinatal optic nerve is downregulated, resulting in a marked decrease in astrocyte proliferation. Oligodendrocyte precursor migration from the brain into the nerve, as well as myelination, was also delayed in the absence of Shh signaling. Conclusions: RGC–derived Shh signaling is required in vivo for maintenance of astrocyte proliferation, as well as normal oligodendrocyte development in the optic nerve.
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