Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

Experimental & Molecular Medicine
Young Ki ChoiHyunggee Kim

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 p...Continue Reading

Citations

Sep 18, 2010·Cell and Tissue Research·Catherine J SandersPaul G Thomas
May 12, 2007·Journal of Virology·Arnaud AutretBruno Blondel
Mar 17, 2009·Experimental & Molecular Medicine·Hye-Jin ChoiJoong-Soo Han
Oct 25, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Niannian Fan, Jiantao Wang
Jun 6, 2014·Journal of Virology·Samantha B KasloffIlaria Capua
Nov 3, 2007·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Jong-Seok KimByung-Doo Hwang

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis