Parkin interacts with Mitofilin to increase dopaminergic neuron death in response to Parkinson's disease-related stressors.

ABSTRACT: Mitochondrial dysfunction plays a critical role in the pathophysiology of Parkinson's disease (PD). The inner mitochondrial membrane (IMM) protein, Mitofilin or Mic60, has been shown to play a key role in controlling and maintaining mitochondrial cristae morphology, and its dysregulation induces cyto-deleterious effects. Here, we investigated the mechanism underlying Mitofilin degradation in dopaminergic neuron death using N27-A cells, and Human Dopamine Neuronal Primary cells treated with PD stressors, Dopamine (DA) or Rotenone (Rot). We found that both PD stressors increased mitochondrial Parkin translocation and interaction with Mitofilin that promotes Mitofilin degradation via ubiquitination, which is responsible for reduced mitochondrial membrane potential and increased ROS pro

SUBMITTER: Imam Aliagan AD 

PROVIDER: S-EPMC7724356 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature