Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP⁺-induced neuronal death.

ABSTRACT: Parkinson's disease (PD) is a chronic neurodegenerative disease with no cure. Calbindin, a Ca²⁺-buffering protein, has been suggested to have a neuroprotective effect in the brain tissues of PD patients and in experimental models of PD. However, the underlying mechanisms remain elusive. Here, we report that in 1-methyl-4-phenylpyridinium (MPP⁺)-induced culture models of PD, the buffering of cytosolic Ca²⁺ by calbindin-D28 overexpression or treatment with a chemical Ca²⁺ chelator reversed impaired autophagic flux, protecting cells against MPP⁺-mediated neurotoxicity. When cytosolic Ca²⁺ overload caused by MPP⁺ was ameliorated, the MPP⁺-induced accumulation of autophagosomes decreased and the autophagic f

SUBMITTER: Jung S 

PROVIDER: S-EPMC6700189 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature