Mitochondria-Targeted Apoptosis in Human Cytomegalovirus-Infected Cells

Mitochondria often play central roles in apoptotic pathways, and disruption of the mitochondrial transmembrane potential (ΔΨm) has been observed in various cells undergoing apoptosis. Human cytomegalovirus (HCMV) infection induces apoptosis in permissive cells; however, investigations of mitochondri...

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Published inJournal of microbiology and biotechnology Vol. 23; no. 11; pp. 1627 - 1635
Main Authors Lee, G.C., K-water, Daejeon, Republic of Korea, Lee, J.H., Kwandong University, Seoul, Republic of Korea, Kim, B.Y., Chungbuk National University, Cheongju, Republic of Korea, Lee, C.H., Chungbuk National University, Cheongju, Republic of Korea
Format Journal Article
LanguageEnglish
Published Seoul Korean Society for Applied Microbiology 01.11.2013
한국미생물·생명공학회
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Summary:Mitochondria often play central roles in apoptotic pathways, and disruption of the mitochondrial transmembrane potential (ΔΨm) has been observed in various cells undergoing apoptosis. Human cytomegalovirus (HCMV) infection induces apoptosis in permissive cells; however, investigations of mitochondria-targeted apoptosis in HCMV-infected human foreskin fibroblast (HFF) cells have been limited. Here, we investigated the mitochondrial apoptosis pathway in HCMV-infected HFF cells. Flow cytometry analysis using JC-1 revealed that HCMV infection induces disruption of ΔΨm in HFF cells when administered 24 h postinfection (hpi), and this disruption was maximized at 48 hpi. Moreover, cytochrome c, normally a mitochondrial inner membrane protein, was detected in cytoplasmic extracts of HCMV-infected cells, but not mock-infected cells, by western blot analysis at 24 hpi. A caspase activity assay based on fluorescence spectrophotometry using a fluorogenic substrate revealed an increase in caspase-3 activity at 48 hpi in HCMV-infected cells. Caspase-8 activity was increased at 72 hpi in HCMV-infected cells. These results imply that HCMV infection induces mitochondria-mediated apoptosis in HFF cells.
Bibliography:A50
G704-000169.2013.23.11.003
ISSN:1017-7825
1738-8872
DOI:10.4014/jmb.1306.06023