Published in
Springer Nature [academic journals on nature.com], Cell Death and Disease, 5(5), p. e1265-e1265, 2014
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Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes
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Marta Vomero,
Cristiano Alessandri,
C. Barbati,
A. Maselli,
Cristina Camperio,
Fabrizio Conti,
A. Tinari,
C. Carlo-Stella,
Loretta Tuosto,
Dario Benincasa,
Guido Valesini,
W. Malorni,
M. Pierdominici,
E. Ortona
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Abstract
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.