Document Detail

Response of HEK293 and CHO cells overexpressing fusiogenic syncytin-1 to mitochondrion-mediated apoptosis induced by antimycin A.
MedLine Citation:
PMID:  18712755     Owner:  NLM     Status:  MEDLINE    
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.
Ina Knerr; Stephan Söder; Elke Licha; Thomas Aigner; Wolfgang Rascher
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  105     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-02     Completed Date:  2008-12-31     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  766-75     Citation Subset:  IM    
Copyright Information:
(c) 2008 Wiley-Liss, Inc.
Children's and Adolescents' Hospital, University of Erlangen-Nuremberg, Erlangen, Germany.
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MeSH Terms
Antimycin A / pharmacology*
Apoptosis* / drug effects
CHO Cells
Caspase 9 / metabolism
Cell Fusion
Cells, Cultured
Gene Products, env / analysis,  genetics,  metabolism*
Microscopy, Confocal
Mitochondria / metabolism*
Pregnancy Proteins / analysis,  genetics,  metabolism*
Reg. No./Substance:
0/Gene Products, env; 0/Pregnancy Proteins; 0/syncytin; 642-15-9/Antimycin A; EC 3.4.22.-/Caspase 9

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