Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells

Vesicular Stomatitis Virus (VSV) has been shown to induce apoptosis in a caspase-dependent manner, but the precise apoptotic pathway remains unknown. We found that caspases 9 and 3, but not caspase 8, were activated during VSV-induced apoptosis in infected Vero cells. Since caspase 9 is related to t...

Descripción completa

Guardado en:

Detalles Bibliográficos
Publicado:	2005
Materias:	AIF Apoptosis Bcl-2 family proteins Caspases Cytochrome c Mitochondrial transmembrane potential VSV apoptosis inducing factor caspase 3 caspase 8 caspase 9 cytochrome c protein Bax protein bcl 2 protein bcl xl animal cell apoptosis article controlled study enzyme activation enzyme activity host pathogen interaction in vitro study membrane potential mitochondrial membrane mitochondrion nonhuman priority journal protein secretion RNA virus signal transduction Vero cell Vesicular stomatitis virus virus infection
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01681702_v109_n1_p65_Gadaleta http://hdl.handle.net/20.500.12110/paper_01681702_v109_n1_p65_Gadaleta
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_01681702_v109_n1_p65_Gadaleta
record_format	dspace
spelling	paper:paper_01681702_v109_n1_p65_Gadaleta2023-06-08T15:17:35Z Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells AIF Apoptosis Bcl-2 family proteins Caspases Cytochrome c Mitochondrial transmembrane potential VSV apoptosis inducing factor caspase 3 caspase 8 caspase 9 cytochrome c protein Bax protein bcl 2 protein bcl xl animal cell apoptosis article controlled study enzyme activation enzyme activity host pathogen interaction in vitro study membrane potential mitochondrial membrane mitochondrion nonhuman priority journal protein secretion RNA virus signal transduction Vero cell Vesicular stomatitis virus virus infection Vesicular stomatitis virus Vesicular Stomatitis Virus (VSV) has been shown to induce apoptosis in a caspase-dependent manner, but the precise apoptotic pathway remains unknown. We found that caspases 9 and 3, but not caspase 8, were activated during VSV-induced apoptosis in infected Vero cells. Since caspase 9 is related to the mitochondrial apoptotic pathway, we analyzed some mitochondrial events such as changes in the mitochondrial transmembrane potential (Δψm) and mitochondrial release of apoptogenic proteins such as cytochrome c and the apoptosis inducing factor (AIF). We found that VSV infection triggers the dissipation of the Δψm and the release of both cytochrome c and AIF from the mitochondrial intermembrane space very early in the VSV infection. These results indicate that the trigger of apoptosis in VSV-infected cells occurs through the early activation of the mitochondrial apoptotic pathway. On the other hand, intracellular levels of the anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, and the pro-apoptotic protein Bax, were assessed during viral infection. These analyses showed that as viral infection proceeded, the cellular level of Bcl-xL decreased, while the levels of Bax and Bcl-2 remained unaffected. The significance of the Bcl-xL modulation is also discussed. © 2004 Elsevier B.V. All rights reserved. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01681702_v109_n1_p65_Gadaleta http://hdl.handle.net/20.500.12110/paper_01681702_v109_n1_p65_Gadaleta
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	AIF Apoptosis Bcl-2 family proteins Caspases Cytochrome c Mitochondrial transmembrane potential VSV apoptosis inducing factor caspase 3 caspase 8 caspase 9 cytochrome c protein Bax protein bcl 2 protein bcl xl animal cell apoptosis article controlled study enzyme activation enzyme activity host pathogen interaction in vitro study membrane potential mitochondrial membrane mitochondrion nonhuman priority journal protein secretion RNA virus signal transduction Vero cell Vesicular stomatitis virus virus infection Vesicular stomatitis virus
spellingShingle	AIF Apoptosis Bcl-2 family proteins Caspases Cytochrome c Mitochondrial transmembrane potential VSV apoptosis inducing factor caspase 3 caspase 8 caspase 9 cytochrome c protein Bax protein bcl 2 protein bcl xl animal cell apoptosis article controlled study enzyme activation enzyme activity host pathogen interaction in vitro study membrane potential mitochondrial membrane mitochondrion nonhuman priority journal protein secretion RNA virus signal transduction Vero cell Vesicular stomatitis virus virus infection Vesicular stomatitis virus Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
topic_facet	AIF Apoptosis Bcl-2 family proteins Caspases Cytochrome c Mitochondrial transmembrane potential VSV apoptosis inducing factor caspase 3 caspase 8 caspase 9 cytochrome c protein Bax protein bcl 2 protein bcl xl animal cell apoptosis article controlled study enzyme activation enzyme activity host pathogen interaction in vitro study membrane potential mitochondrial membrane mitochondrion nonhuman priority journal protein secretion RNA virus signal transduction Vero cell Vesicular stomatitis virus virus infection Vesicular stomatitis virus
description	Vesicular Stomatitis Virus (VSV) has been shown to induce apoptosis in a caspase-dependent manner, but the precise apoptotic pathway remains unknown. We found that caspases 9 and 3, but not caspase 8, were activated during VSV-induced apoptosis in infected Vero cells. Since caspase 9 is related to the mitochondrial apoptotic pathway, we analyzed some mitochondrial events such as changes in the mitochondrial transmembrane potential (Δψm) and mitochondrial release of apoptogenic proteins such as cytochrome c and the apoptosis inducing factor (AIF). We found that VSV infection triggers the dissipation of the Δψm and the release of both cytochrome c and AIF from the mitochondrial intermembrane space very early in the VSV infection. These results indicate that the trigger of apoptosis in VSV-infected cells occurs through the early activation of the mitochondrial apoptotic pathway. On the other hand, intracellular levels of the anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, and the pro-apoptotic protein Bax, were assessed during viral infection. These analyses showed that as viral infection proceeded, the cellular level of Bcl-xL decreased, while the levels of Bax and Bcl-2 remained unaffected. The significance of the Bcl-xL modulation is also discussed. © 2004 Elsevier B.V. All rights reserved.
title	Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
title_short	Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
title_full	Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
title_fullStr	Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
title_full_unstemmed	Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells
title_sort	early activation of the mitochondrial apoptotic pathway in vesicular stomatitis virus-infected cells
publishDate	2005
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01681702_v109_n1_p65_Gadaleta http://hdl.handle.net/20.500.12110/paper_01681702_v109_n1_p65_Gadaleta
_version_	1768545184660848640

Early activation of the mitochondrial apoptotic pathway in Vesicular Stomatitis Virus-infected cells

Ejemplares similares