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.
Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes / Colasanti, Tania; Vomero, Marta; Alessandri, Cristiano; Barbati, Cristiana; A., Maselli; Camperio, Cristina; Conti, Fabrizio; A., Tinari; C., Carlo Stella; Tuosto, Loretta; Benincasa, Dario; Valesini, Guido; W., Malorni; M., Pierdominici; E., Ortona. - In: CELL DEATH & DISEASE. - ISSN 2041-4889. - ELETTRONICO. - 5:(2014), p. e1265. [10.1038/cddis.2014.211]
Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes
COLASANTI, TANIA;VOMERO, MARTA;ALESSANDRI, cristiano;BARBATI, CRISTIANA;CAMPERIO, Cristina;CONTI, FABRIZIO;TUOSTO, Loretta;BENINCASA, DARIO;VALESINI, Guido;
2014
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.