It has been demonstrated that α-synuclein can aggregate and contribute to the pathogenesis of some neurodegenerative diseases and it is capable of hindering autophagy in neuronal cells. Here, we investigated the implication of α-synuclein in the autophagy process in primary human T lymphocytes. We provide evidence that: (i) knocking down of the α-synuclein gene resulted in increased autophagy, (ii) autophagy induction by energy deprivation was associated with a significant decrease of α-synuclein levels, (iii) autophagy inhibition by 3-methyladenine or by ATG5 knocking down led to a significant increase of α-synuclein levels, and (iv) autophagy impairment, constitutive in T lymphocytes from patients with systemic lupus erythematosus, was associated with abnormal accumulation of α-synuclein aggregates. These results suggest that α-synuclein could be considered as an autophagy-related marker of peripheral blood lymphocytes, potentially suitable for use in the clinical practice.
|Titolo:||Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes|
|Parole Chiave:||adult; aged; biological markers; female; gene knockdown techniques; humans; lupus erythematosus, systemic; male; middle aged; T-lymphocytes; alpha-synuclein; autophagy|
|Settore Scientifico Disciplinare:||Settore MED/15 - Malattie del Sangue|
|Data di pubblicazione:||mag-2014|
|Digital Object Identifier (DOI):||10.1038/cddis.2014.211|
|Appare nelle tipologie:||01 - Articolo su periodico|