rotenone upregulates alpha-synuclein and myocyte enhancer factor 2d independently from lysosomal degradation inhibition

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ID: 143590
2013
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Abstract
Dysfunctions of chaperone-mediated autophagy (CMA), the main catabolic pathway for alpha-synuclein, have been linked to the pathogenesis of Parkinson’s disease (PD). Since till now there is limited information on how PD-related toxins may affect CMA, in this study we explored the effect of mitochondrial complex I inhibitor rotenone on CMA substrates, alpha-synuclein and MEF2D, and effectors, lamp2A and hsc70, in a human dopaminergic neuroblastoma SH-SY5Y cell line. Rotenone induced an upregulation of alpha-synuclein and MEF2D protein levels through the stimulation of their de novo synthesis rather than through a reduction of their CMA-mediated degradation. Moreover, increased MEF2D transcription resulted in higher nuclear protein levels that exert a protective role against mitochondrial dysfunction and oxidative stress. These results were compared with those obtained after lysosome inhibition with ammonium chloride. As expected, this toxin induced the cytosolic accumulation of both alpha-synuclein and MEF2D proteins, as the result of the inhibition of their lysosome-mediated degradation, while, differently from rotenone, ammonium chloride decreased MEF2D nuclear levels through the downregulation of its transcription, thus reducing its protective function. These results highlight that rotenone affects alpha-synuclein and MEF2D protein levels through a mechanism independent from lysosomal degradation inhibition.
Reference Key
sala2013biomedrotenone Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Gessica Sala;Alessandro Arosio;Giovanni Stefanoni;Laura Melchionda;Chiara Riva;Daniele Marinig;Laura Brighina;Carlo Ferrarese
Journal spectrochimica acta - part a: molecular and biomolecular spectroscopy
Year 2013
DOI
10.1155/2013/846725
URL
http://dx.doi.org/10.1155/2013/846725
Keywords
Medicine

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