Expression and regulation of the mu opioid peptide receptor in TPA-differentiated HL-60 promyelocytic leukemia cells

    loading  Checking for direct PDF access through Ovid

Abstract

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.

Related Topics

    loading  Loading Related Articles