Document Detail


Morphine suppresses lymphocyte apoptosis by blocking p53-mediated death signaling.
MedLine Citation:
PMID:  12927789     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Opiates such as morphine or heroin may promote cell apoptosis and cause dysfunction of immune cells. In simian immunodeficiency virus (SIV)-infected lymphocytic cells, however, morphine may protect the cells from apoptotic lysis and allow the virus to continue to replicate. To further explore this apparently antithetical effect of opiates, we evaluated in the present study the effects of morphine on human lymphocytic CEM x174 cells induced to undergo apoptosis in the presence of actinomycin D. It was found that induction of apoptosis (characterized by DNA laddering) by actinomycin D was accompanied by a stimulation of the expression of active (phosphorylated) form of p53. Pretreatment of the cells with 10nM morphine caused a transient, naloxone-reversible suppression of the appearance of activated p53 and the generation of DNA laddering. Parallel evaluation of the growth of CEM x174 indicated that morphine treatment delays the inception of cell death triggered by actinomycin D. Inasmuch as Bcl-2 suppresses while Bax accelerates apoptosis, treatment of cells with morphine reduced the expression of Bax and enhanced the expression of Bcl-2. Taken together, morphine, through binding at the opioid receptor, may protect lymphocytic cells from apoptotic lysis if cell death is initiated by apoptosis-inducing agents such as human immunodeficiency virus (HIV), SIV or actinomycin D.
Authors:
Shunji Suzuki; Linda F Chuang; Roy H Doi; Ronald Y Chuang
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  308     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-20     Completed Date:  2003-10-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  802-8     Citation Subset:  IM    
Affiliation:
Department of Medical Pharmacology and Toxicology, School of Medicine, University of California, Davis, CA 95616, USA.
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MeSH Terms
Descriptor/Qualifier:
Analgesics, Opioid / pharmacology
Apoptosis / drug effects*
Blotting, Western
Cell Death
Cell Survival
Dactinomycin / pharmacology
Electrophoresis, Polyacrylamide Gel
Humans
Lymphocytes / pathology*
Models, Biological
Morphine / pharmacology*
Naloxone / pharmacology
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
Receptors, Opioid, mu / metabolism
Retinoblastoma Protein / metabolism
Signal Transduction / drug effects
Time Factors
Tumor Suppressor Protein p53 / metabolism*
bcl-2-Associated X Protein
Grant Support
ID/Acronym/Agency:
DA 05901/DA/NIDA NIH HHS; DA 10433/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Analgesics, Opioid; 0/BAX protein, human; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Opioid, mu; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53; 0/bcl-2-Associated X Protein; 465-65-6/Naloxone; 50-76-0/Dactinomycin; 57-27-2/Morphine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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