Data/hora: 05/06/2024 07:30:42

Provedor de dados: | 74
País: | Brazil
Título: | Glutathione depletion triggers actin cytoskeleton changes via actin-binding proteins
Autores: | Zepeta-Flores,Nahum; Valverde,Mahara; Lopez-Saavedra,Alejandro; Rojas,Emilio.
Data: | 2018-06-01
Ano: | 2018
Palavras-chave: | Glutathione; BSO; Thymosin β4; Gelsolin; Profiling.
Resumo: | Abstract The importance of glutathione (GSH) in alternative cellular roles to the canonically proposed, were analyzed in a model unable to synthesize GSH. Gene expression analysis shows that the regulation of the actin cytoskeleton pathway is strongly impacted by the absence of GSH. To test this hypothesis, we evaluate the effect of GSH depletion via buthionine sulfoximine (5 and 12.5 mM) in human neuroblastoma MSN cells. In the present study, 70% of GSH reduction did not induce reactive oxygen species, lipoperoxidation, or cytotoxicity, which enabled us to evaluate the effect of glutathione in the absence of oxidative stress. The cells with decreasing GSH levels acquired morphology changes that depended on the actin cytoskeleton and not on tubulin. We evaluated the expression of three actin-binding proteins: thymosin β4, profilin and gelsolin, showing a reduced expression, both at gene and protein levels at 24 hours of treatment; however, this suppression disappears after 48 hours of treatment. These changes were sufficient to trigger the co-localization of the three proteins towards cytoplasmic projections. Our data confirm that a decrease in GSH in the absence of oxidative stress can transiently inhibit the actin binding proteins and that this stimulus is sufficient to induce changes in cellular morphology via the actin cytoskeleton.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572018000300475
Editor: | Sociedade Brasileira de Genética
Relação: | 10.1590/1678-4685-gmb-2017-0158
Formato: | text/html
Fonte: | Genetics and Molecular Biology  v.41 n.2 2018
Fonte: | info:eu-repo/semantics/openAccess