| Response of HEK293 and CHO cells overexpressing fusiogenic syncytin-1 to mitochondrion-mediated apoptosis induced by antimycin A. | |
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MedLine Citation:
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PMID: 18712755 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis is essential for the regulation of cellular homeostasis in the placenta and is also involved in the pathophysiology of pregnancy-related diseases such as pre-eclampsia and intrauterine growth restriction (IUGR). Syncytin-1, a fusiogenic glycoprotein of endogenous-retroviral origin expressed in human trophoblasts, facilitates placental syncytium formation and is found reduced in pre-eclamptic placentas. We focus here on the mitochondrial apoptotic pathway and investigate whether the overexpression of syncytin-1 in HEK293-52 (human embryonic kidney cells) and CHO-52 cells influences the apoptotic response to the mitochondrial inhibitor antimycin A (AA). After the induction of apoptosis by 5 microM AA and incubation for up to 36 h in the absence of serum, the mean apoptotic rate was reduced by 15-30% in syncytin-1 transfected cells compared with mock-transfectants. After 12 h of challenge with AA we found lower cytochrome c levels in the cytoplasmic protein fraction and higher amounts in the mitochondrial fraction in syncytin-1 transfectants compared with mock-transfectants. We observed a decreased Mitotracker Red staining of mitochondria following AA challenge for 24 h in mock-treated CHO cells, in particular, compared with syncytin-1 transfectants. Moreover, we found a reduced activation of caspase 9 in syncytin-1 transfected HEK293-52 cells after 48 h of apoptotic challenge compared to mock-transfectants. However, a high expression of anti-apoptotic Bcl-x(L) was found in both cell types. Using syncytin-1 transfected HEK293-52 cells and CHO-52 cells, we provide initial evidence that syncytin-1 may exert its anti-apoptotic function at the mitochondrial level. A reduced release of cytochrome c followed by a diminished activation of caspase 9 is a possible mechanism. |
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Authors:
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Ina Knerr; Stephan Söder; Elke Licha; Thomas Aigner; Wolfgang Rascher |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cellular biochemistry Volume: 105 ISSN: 1097-4644 ISO Abbreviation: J. Cell. Biochem. Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-10-02 Completed Date: 2008-12-31 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8205768 Medline TA: J Cell Biochem Country: United States |
Other Details:
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Languages: eng Pagination: 766-75 Citation Subset: IM |
Copyright Information:
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(c) 2008 Wiley-Liss, Inc. |
Affiliation:
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Children's and Adolescents' Hospital, University of Erlangen-Nuremberg, Erlangen, Germany. ina.knerr@uk-erlangen.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antimycin A / pharmacology* Apoptosis* / drug effects CHO Cells Caspase 9 / metabolism Cell Fusion Cells, Cultured Cricetinae Cricetulus Gene Products, env / analysis, genetics, metabolism* Humans Microscopy, Confocal Mitochondria / metabolism* Pregnancy Proteins / analysis, genetics, metabolism* Transfection |
| Chemical | |
Reg. No./Substance:
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0/Gene Products, env; 0/Pregnancy Proteins; 0/syncytin; 642-15-9/Antimycin A; EC 3.4.22.-/Caspase 9 |
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