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

Beltrán, José Eduardo Padilla; Peek, Jennifer L; Chang, Sulie L.

doi:10.1016/j.intimp.2006.03.017

Cited by 16 publications

(16 citation statements)

References 28 publications

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“…In the present study up-regulation of the MOR expression at the transcriptional level was observed in the rostral brain and hypothalamus of HIV-1 Tg rats, along with increased opioid agonist potency. Functional supersensitivity to opioid agonists is also seen following opioid antagonist-induced upregulation [54,55] as predicted by drug receptor theory [56] . Studies with MOR knock out mice demonstrate that MOR mediates both the analgesic and rewarding or addictive properties of morphine [57] .…”

Section: Mu Opioid Receptor Expression In Hiv-1 Tg Rat Brain Areasmentioning

confidence: 86%

Role of HIV-1 Infection in Addictive Behavior: A Study of a HIV-1 Transgenic Rat Model

Chang¹,

Vigorito²

2006

American J. of Infectious Diseases

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Epidemiological research indicates that drug abuse is prevalent among individuals infected with HIV-1. Evidence from preclinical research also suggests that drugs of abuse exacerbate the progression of neuropathological changes in the HIV-1 infected brain probably through common mechanisms of neuronal injury. The effects of HIV-1 on the efficacy and abuse potential of controlled drugs such as morphine, however, has not been explored. The current study reports that the noninfectious HIV-1 transgenic (HIV-1 Tg) rat shows up-regulated expression of the mu opioid receptor (MOR) at the transcriptional level and functional supersensitivity to morphine, a MOR agonist. Compared to nontransgenic control rats, the HIV-1 Tg rats also show greater motivation to run in a wheel, a behavior that is known to be associated with increased drug self-administration. These results suggest the potential role of HIV-1 infection in enhancing vulnerability to addiction and this possibility warrants further investigation to better understand the link between HIV-1 infection and the abuse of drugs including opioids.

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Section: Mu Opioid Receptor Expression In Hiv-1 Tg Rat Brain Areasmentioning

confidence: 86%

Role of HIV-1 Infection in Addictive Behavior: A Study of a HIV-1 Transgenic Rat Model

Chang¹,

Vigorito²

2006

American J. of Infectious Diseases

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“…In addition to treatment of opioid withdrawal, methadone is of significant use as a long-acting analgesic, particularly for neuropathic pain syndromes (4)(5)(6). Leukemia cells such as HL-60 cells express the A opioid peptide receptor, which was regulated by morphine (19). Anticancer drugs induce apoptosis in leukemias and solid tumors (1).…”

Section: Discussionmentioning

confidence: 99%

Methadone, Commonly Used as Maintenance Medication for Outpatient Treatment of Opioid Dependence, Kills Leukemia Cells and Overcomes Chemoresistance

et al. 2008

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The therapeutic opioid drug methadone (D,L-methadone hydrochloride) is the most commonly used maintenance medication for outpatient treatment of opioid dependence. In our study, we found that methadone is also a potent inducer of cell death in leukemia cells and we clarified the unknown mechanism of methadone-induced cell killing in leukemia cells. Methadone inhibited proliferation in leukemia cells and induced cell death through apoptosis induction and activated apoptosis pathways through the activation of caspase-9 and caspase-3, down-regulation of Bcl-x L and X chromosome-linked inhibitor of apoptosis, and cleavage of poly(ADP-ribose) polymerase. In addition, methadone induced cell death not only in anticancer drug-sensitive and apoptosis-sensitive leukemia cells but also in doxorubicinresistant, multidrug-resistant, and apoptosis-resistant leukemia cells, which anticancer drugs commonly used in conventional therapies of leukemias failed to kill. Depending on caspase activation, methadone overcomes doxorubicin resistance, multidrug resistance, and apoptosis resistance in leukemia cells through activation of mitochondria. In contrast to leukemia cells, nonleukemic peripheral blood lymphocytes survived after methadone treatment. These findings show that methadone kills leukemia cells and breaks chemoresistance and apoptosis resistance. Our results suggest that methadone is a promising therapeutic approach not only for patients with opioid dependence but also for patients with leukemias and provide the foundation for new strategies using methadone as an additional anticancer drug in leukemia therapy, especially when conventional therapies are less effective. [Cancer Res 2008;68(15):6059-64]

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“…The HL-60 cells were treated with 16 nM TPA in a control vehicle of 0.1% ethanol for 4 days. The cell culture medium containing TPA was changed every 48 h until the cells were differentiated into macrophage/monocytic-like cells (5), which were designated as TPA-HL-60 cells (3,4).…”

Section: Methodsmentioning

confidence: 99%

“…HL-60 promyelocytic leukemia cells are well-characterized, immortal cells capable of differentiating into macrophage-like cells by treatment with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) (4,5). We previously reported that MOR is expressed in TPA-differentiated HL-60 (TPA-HL-60) cells, and recently we showed that HIV gp120 induces the secretion of TNF-␣ from these cells, which then up-regulates the expression of the MOR in an autocrine/paracrine manner (3).…”

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confidence: 99%

Expression of the Mu Opioid Receptor in the Human Immunodeficiency Virus Type 1 Transgenic Rat Model

Chang

Beltrán

Swarup

2007

J Virol

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

Cited by 16 publications

References 28 publications

Role of HIV-1 Infection in Addictive Behavior: A Study of a HIV-1 Transgenic Rat Model

Role of HIV-1 Infection in Addictive Behavior: A Study of a HIV-1 Transgenic Rat Model

Methadone, Commonly Used as Maintenance Medication for Outpatient Treatment of Opioid Dependence, Kills Leukemia Cells and Overcomes Chemoresistance

Expression of the Mu Opioid Receptor in the Human Immunodeficiency Virus Type 1 Transgenic Rat Model

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