Neuroprotective effect and adult optic nerve regeneration of administration of tacrolimus against spontaneous neuropathy in NF-kBp50-dificient mice as a normal tension glaucoma model

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The transcription factor nuclear factor-kappa B (NF-kB)/Rel family may be involved in neuronal cell death and survival. We reported that NF -kBp50-deficient mice exhibit many features resembling human normal tension glaucoma (NTG). Our aim is to elucidate the mechanism of the initiation of NTG. Chronic optic neuropathy was significantly reduced under chronic administration of calcineurin inhibitor Tacrolimus. We have also investigated whether retinal cells have the potential to generate neurons in p50-deficient mice with chronic administration of Tacrolimus. Tacrolimus-treatment markedly promotes the proliferation of bipolar cell-derived retinal progenitors and optic nerve regeneration after damage to or during the degeneration of retinal ganglion cells in p50-deficient mice.These experimental results proposed optic nerve healing and basic fibroblast growth factor (bFGF) expression by the chronic administration of Tacrolimus.