Human retinoic acid receptor-related orphan receptor alpha1 overexpression protects neurones against oxidative stress-induced apoptosis.

摘要: Retinoic acid receptor-related orphan receptor alpha (RORalpha) is a transcription factor belonging to the superfamily of nuclear receptors. Disruption Rora gene in mouse results defect development Purkinje cells leading cerebellar atrophy, which suggests neuroprotective role for RORalpha. To test this hypothesis, survival rate lentiviral-mediated human RORalpha1-overexpressing neurones has been evaluated response different stressors disturbing redox homeostasis, such as beta-amyloid peptide, c(2)-ceramide and H(2)O(2). We show that overexpression RORalpha1 provides neuroprotection by increasing expression antioxidant proteins glutathione peroxidase 1 peroxiredoxin 6, reduction accumulation stress-induced reactive oxygen species. further demonstrate effect RORalpha predominantly mediated 6. These suggest new control neuronal oxidative stress thus represents interest regulation species-induced neurodegenerative processes during ageing.