Document Detail

The Fas/FasL apoptotic pathway is involved in kappa-opioid-induced apoptosis of human endometrial stromal cells.
MedLine Citation:
PMID:  11517294     Owner:  NLM     Status:  MEDLINE    
Human endometrium expresses specific kappa-opioid binding sites and their endogenous ligands, the dynorphins. In neural crest-derived tissues, kappa-opioids affect apoptosis, a phenomenon of major significance in endometrial stroma physiology. Our hypothesis was that endometrial kappa-opioids may play a role in endometrial stromal cell apoptosis. Thus, we examined the effect of the synthetic kappa-opioid agonist, U69593, on the apoptotic rate of human endometrial stromal cells in primary culture. Apoptosis of endometrial stromal cells was elevated after 3 h exposure to 100 nmol/l U69593, and remained elevated for up to 3 days. This effect was dose-dependent and was reversed by the general opioid antagonist, naloxone, suggesting that it is mediated via opioid receptors. In parallel, semi-quantitative Western blot and flow cytometry analysis showed that U69593 caused a rapid but transient up-regulation of Fas protein, suggesting that its effect on apoptosis is mediated by activation of the Fas/FasL apoptotic pathway. Additionally, U69593 increased the content of the anti-apoptotic members of the Bcl-2 family of proteins, the Bcl-2 and Bcl-x(L), whereas it had no significant effect on the apoptosis-promoting homologues Bax, Bcl-x(S) and Bak. This implies that a transient survival mechanism is activated in stromal cells as a parallel rescue response to the apoptosis-inducing factor. In conclusion, our data suggest that endometrial opioid dynorphins may participate in the apoptotic processes related to endometrial tissue remodelling during early pregnancy or menstruation.
E Chatzaki; A Makrigiannakis; A N Margioris; E Kouimtzoglou; A Gravanis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular human reproduction     Volume:  7     ISSN:  1360-9947     ISO Abbreviation:  Mol. Hum. Reprod.     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-08-22     Completed Date:  2001-11-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9513710     Medline TA:  Mol Hum Reprod     Country:  England    
Other Details:
Languages:  eng     Pagination:  867-74     Citation Subset:  IM    
Department of Pharmacology, School of Medicine, University of Crete, Heraklion GR-711 10, Crete, Greece.
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MeSH Terms
Antigens, CD95 / metabolism*
Apoptosis* / drug effects
Cells, Cultured
Endometrium / cytology*,  drug effects
Fas Ligand Protein
Membrane Glycoproteins / physiology*
Proto-Oncogene Proteins c-bcl-2 / metabolism
Pyrrolidines / pharmacology
Receptors, Opioid, kappa / agonists,  physiology*
Signal Transduction* / drug effects
Stromal Cells / cytology,  drug effects
Reg. No./Substance:
0/Antigens, CD95; 0/Benzeneacetamides; 0/FASLG protein, human; 0/Fas Ligand Protein; 0/Ligands; 0/Membrane Glycoproteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Pyrrolidines; 0/Receptors, Opioid, kappa; 96744-75-1/U 69593

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