Document Detail

Expression and regulation of the mu opioid peptide receptor in TPA-differentiated HL-60 promyelocytic leukemia cells.
MedLine Citation:
PMID:  16782547     Owner:  NLM     Status:  MEDLINE    
Cellular differentiation of immune cells involves an array of molecular events responsible for their commitment to cellular maturation. Treatment of HL-60 promyelocytic leukemia cells with 12-o-tetradecanoyl-phorbol-13-acetate (TPA) induces the cells to differentiate into monocyte/macrophage-like cells. In this study, following TPA treatment, there was a significant increase in mu opioid peptide receptor (MOPR) mRNA levels in the differentiated HL-60 cells as measured by quantitative-competitive RT-PCR (QC-RT-PCR) and real-time RT-PCR. Morphine's inhibition of forskolin-induced intracellular cAMP confirmed the functionality of the MOPR. TPA-induced differentiation also significantly enhanced the binding activities of two transcriptional factors, AP-1 and NFkB. Prolonged treatment of the TPA-differentiated HL-60 cells with morphine down-regulated MOPR mRNA expression and decreased the binding activities of AP-1 and NFkB, both of which were naloxone reversible. Thus, the direct correlation between AP-1 and NFkB binding activities and MOPR expression in HL-60 cells following TPA-induced differentiation as well as in TPA-differentiated HL-60 cells given prolonged treatment with morphine suggests that transcriptional factors, such as AP-1 and NFkB, may play a role in the molecular mechanisms underlying regulation of MOPR expression in immune cells.
Jose A Beltran; Jennifer Peek; Sulie L Chang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-05-19
Journal Detail:
Title:  International immunopharmacology     Volume:  6     ISSN:  1567-5769     ISO Abbreviation:  Int. Immunopharmacol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-06-19     Completed Date:  2006-09-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100965259     Medline TA:  Int Immunopharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1331-40     Citation Subset:  IM    
Department of Biology, Seton Hall University, McNulty Hall, Room 215, South Orange, NJ 07079, USA.
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MeSH Terms
Analgesics, Opioid / pharmacology
Cyclic AMP / metabolism
Forskolin / pharmacology
Gene Expression Regulation, Leukemic / drug effects*
HL-60 Cells
Morphine / pharmacology
NF-kappa B / metabolism
Naloxone / pharmacology
Narcotic Antagonists / pharmacology
Protein Binding / drug effects
RNA, Messenger / genetics,  metabolism
Receptors, Opioid, mu / genetics*
Reverse Transcriptase Polymerase Chain Reaction / methods
Tetradecanoylphorbol Acetate / pharmacology*
Transcription Factor AP-1 / metabolism
Grant Support
K02 DA 016149/DA/NIDA NIH HHS; R01 DA 007058/DA/NIDA NIH HHS
Reg. No./Substance:
0/Analgesics, Opioid; 0/NF-kappa B; 0/Narcotic Antagonists; 0/RNA, Messenger; 0/Receptors, Opioid, mu; 0/Transcription Factor AP-1; 16561-29-8/Tetradecanoylphorbol Acetate; 465-65-6/Naloxone; 57-27-2/Morphine; 60-92-4/Cyclic AMP; 66428-89-5/Forskolin

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

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