Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells.
Fish Shellfish Immunol
; 45(2): 848-57, 2015 Aug.
Article
en En
| MEDLINE
| ID: mdl-26067170
ABSTRACT
The giant seaperch iridovirus (GSIV) induces host cell apoptosis by a poorly-understood process. In this study, GSIV is shown to upregulate the pro-apoptotic death genes Bax and Bak at the middle replication stage, and factors in the grouper fin cell line (GF-1) are shown to modulate this process. Studying the mechanism of cell death, we found that upregulated, de novo-synthesized Bax and Bak proteins formed heterodimers. This up-regulation process correlated with mitochondrial membrane potential (MMP) loss, increased caspase-3 activity, and increased apoptotic cell death. All effects were diminished by treatment of infected GF-1 cells with the protein synthesis inhibitor cycloheximide. Interestingly, overexpression of the anti-apoptotic gene Bcl-xL also diminished GSIV-induced mitochondria-mediated cell death, increasing host cell viability and decreasing MMP loss at the early replication stage. Our data suggest that GSIV induces GF-1 apoptotic cell death through up-regulation of the pro-apoptotic genes Bax and Bak, which are regulated by Bcl-xL overexpression on mitochondria in GF-1 cells.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Lubina
/
Regulación hacia Arriba
/
Proteínas de Peces
/
Infecciones por Virus ADN
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Proteína X Asociada a bcl-2
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Proteína Destructora del Antagonista Homólogo bcl-2
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Enfermedades de los Peces
Límite:
Animals
Idioma:
En
Revista:
Fish Shellfish Immunol
Asunto de la revista:
BIOLOGIA
/
MEDICINA VETERINARIA
Año:
2015
Tipo del documento:
Article
País de afiliación:
Taiwán