Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death
Experimental & Molecular Medicine
; : 11-17, 2006.
Article
em En
| WPRIM
| ID: wpr-77906
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WPRO
ABSTRACT
The mitochondrial pathway of swine influenza virus (SIV)-induced apoptosis was investigated using porcine kidney (PK-15) cells, swine testicle (ST) cells, and HeLa cervical carcinoma cells which are known not to support viral replication. As judged by cell morphology, annexin V staining, and DNA fragmentation, PK-15 and ST cells infected with three different subtypes of SIV (H1N1, H3N2, and H1N2) were obviously killed by apoptosis, not necrosis. SIV infection in PK-15 and HeLa cells was shown to decrease the cellular levels of Bcl-2 protein compared to that of mock-infected control cells at 24 h post-infection, whereas expression levels of Bax protein increased in the PK-15 cells, but did not increase in HeLa cells by SIV infection. Cytochrome c upregulation was also observed in cytosolic fractions of the PK-15 and HeLa cells infected with SIV. Apoptosome (a multi-protein complex consisting of cytochrome c, Apaf-1, caspase-9, and ATP) formation was confirmed by immunoprecipitation using cytochrome c antibody. Furthermore, SIV infection increased the cellular levels of TAJ, an activator of the JNK-stressing pathway, and the c-Jun protein in the PK-15 and HeLa cells. Taken together, these results suggest that the mitochondrial pathway should be implicated in the apoptosis of PK-15 cells induced by SIV infection.
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Assunto principal:
Vírus da Influenza A
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Suínos
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Testes de Precipitina
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Estudo Comparativo
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Cinética
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Células HeLa
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Regulação Viral da Expressão Gênica
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Fracionamento Celular
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Linhagem Celular
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Western Blotting
Limite:
Animals
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Humans
Idioma:
En
Revista:
Experimental & Molecular Medicine
Ano de publicação:
2006
Tipo de documento:
Article