Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/53861
Title: Overexpression of -synuclein in an astrocyte cell line promotes autophagy inhibition and apoptosis
Authors: Erustes, Adolfo Garcia [UNIFESP]
Stefani, Fernanda Yakel [UNIFESP]
Terashima, Juliana Yoshie [UNIFESP]
Stilhano, Roberta Sessa [UNIFESP]
Monteforte, Priscila Totarelli [UNIFESP]
da Silva Pereira, Gustavo Jose [UNIFESP]
Han, Sang Won [UNIFESP]
Calgarotto, Andrana Karla
Hsu, Yi-Te
Ureshino, Rodrigo Portes [UNIFESP]
Bincoletto, Claudia [UNIFESP]
Smaili, Soraya Soubhi [UNIFESP]
Keywords: Parkinson disease
-synuclein
A30P
A53T
parkin
autophagy
Issue Date: 2018
Publisher: Wiley
Citation: Journal Of Neuroscience Research. Hoboken, v. 96, n. 1, p. 160-171, 2018.
Abstract: α‐Synuclein is the major component of neuronal cytoplasmic aggregates called Lewy bodies, the main pathological hallmark of Parkinson disease. Although neurons are the predominant cells expressing α‐synuclein in the brain, recent studies have demonstrated that primary astrocytes in culture also express α‐synuclein and regulate α‐synuclein trafficking. Astrocytes have a neuroprotective role in several detrimental brain conditions; we therefore analyzed the effects of the overexpression of wild‐type α‐synuclein and its A30P and A53T mutants on autophagy and apoptosis. We observed that in immortalized astrocyte cell lines, overexpression of α‐synuclein proteins promotes the decrease of LC3‐II and the increase of p62 protein levels, suggesting the inhibition of autophagy. When these cells were treated with rotenone, there was a loss of mitochondrial membrane potential, especially in cells expressing mutant α‐synuclein. The level of this decrease was related to the toxicity of the mutants because they show a more intense and sustained effect. The decrease in autophagy and the mitochondrial changes in conjunction with parkin expression levels may sensitize astrocytes to apoptosis.
URI: https://repositorio.unifesp.br/handle/11600/53861
ISSN: 0360-4012
Other Identifiers: http://dx.doi.org/10.1002/jnr.24092
Appears in Collections:Artigo

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