Autophagy as a Neuroprotective Mechanism Against 3-Nitropropionic Acid-Induced Murine Astrocyte Cell Death

Autophagy as a Neuroprotective Mechanism Against 3-Nitropropionic Acid-Induced Murine Astrocyte Cell Death

Autor Pereira, Gustavo J. S. Autor UNIFESP Google Scholar
Tressoldi, Nicole Autor UNIFESP Google Scholar
Hirata, Hanako Autor UNIFESP Google Scholar
Bincoletto, Claudia Autor UNIFESP Google Scholar
Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo Huntington's disease (HD) is a genetic neurodegenerative disorder that is characterized by severe striatal atrophy with extensive neuronal loss and gliosis. Although the molecular mechanism is not well understood, experimental studies use the irreversible mitochondrial inhibitor 3-nitropropionic acid (3-NP) to mimic the neuropathological features of HD. in this study, the role of autophagy as a neuroprotective mechanism against 3-NP-induced astrocyte cytotoxicity was evaluated. Autophagy is a catabolic process that is essential for the turnover of cytosolic proteins and organelles and is involved in the modulation of cell death and survival. We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. the upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.
Assunto Huntington's disease
3-Nitropropionic acid
Apoptosis
Autophagy
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Data 2013-11-01
Publicado em Neurochemical Research. New York: Springer/plenum Publishers, v. 38, n. 11, p. 2418-2426, 2013.
ISSN 0364-3190 (Sherpa/Romeo, fator de impacto)
Editor Springer
Extensão 2418-2426
Fonte http://dx.doi.org/10.1007/s11064-013-1154-5
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000325704400020
URI http://repositorio.unifesp.br/handle/11600/36930

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