Mitochondrial Effects of PGC-1alpha Silencing in MPP⁺ Treated Human SH-SY5Y Neuroblastoma Cells.

ABSTRACT: The dopaminergic neuron degeneration and loss that occurs in Parkinson's disease (PD) has been tightly linked to mitochondrial dysfunction. Although the aged-related cause of the mitochondrial defect observed in PD patients remains unclear, nuclear genes are of potential importance to mitochondrial function. Human peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) is a multi-functional transcription factor that tightly regulates mitochondrial biogenesis and oxidative capacity. The goal of the present study was to explore the potential pathogenic effects of interference by the PGC-1α gene on N-methyl-4-phenylpyridinium ion (MPP⁺)-induced SH-SY5Y cells. We utilized RNA interference (RNAi) technology to probe the pathogenic consequences of inhibiting PGC-1α in

SUBMITTER: Ye Q 

PROVIDER: S-EPMC5447087 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature