κ-Opioid Receptor Ligands Inhibit Cocaine-Induced HIV-1 Expression in Microglial Cells

Gekker, Genya; Hu, Shuxian; Wentland, Mark P.; Bidlack, Jean M.; Lokensgard, James R.; Peterson, Phillip K.

doi:10.1124/jpet.103.060160

Cited by 39 publications

(34 citation statements)

References 38 publications

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“…With progression of HIV-1, infections patients subsequently can develop HIVE (Gendelman et al, 1994;Li et al, 2005). Previous studies have shown that drugs of abuse such as cocaine enhance the replication of HIV-1 in vitro (Bagasra and Pomerantz, 1993;Gekker et al, 2004;Nair et al, 2005;Peterson et al, 1991;Peterson et al, 1992;Peterson et al, 1993), supporting the hypothesis that drug abuse is a co-factor in the pathogenesis of HIV-1 disease. The current study demonstrates that pretreatment of NHA with cocaine prior to HIV-1 infection enhances viral replication as demonstrated by a significant increase in LTR-R/U5 gene expression as well as increased p24 antigen levels compared to the non-cocaine treated HIV-1 infection control.…”

Section: Discussionsupporting

confidence: 51%

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

et al. 2006

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The US is experiencing an epidemic of cocaine use entangled with HIV-1 infection. Normal human astrocytes (NHA) are susceptible to HIV-1 infection. We utilized LTR-R/U5 amplification, p24 antigen assay and the proteomic method of difference gel electrophoresis (DIGE) combined with protein identification through HPLC-MS/MS to investigate the effect of cocaine on HIV-1 infectivity and the proteomic profile of NHA, respectively. Data demonstrate that cocaine significantly upregulates HIV-1 infection in NHA as measured by LTR-R/U5 amplification and p24 antigen assay. Further, our results show for the first time that cocaine differentially regulates the expression of a number of proteins by NHA that may play a role in the neuropathogenesis of HIV-1 disease.

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Section: Discussionsupporting

confidence: 51%

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

et al. 2006

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“…Previous studies have shown that drugs of abuse such as cocaine enhance the replication of HIV-1 in vitro [47][48][49][50][51] supporting the hypothesis that drug abuse is a cofactor in the pathogenesis of HIV-1 disease. Studies by Gavrilin et al [52] demonstrate that METH significantly increases feline immunodeficiency virus (FIV, X4) replication in astrocytes [52].…”

Section: Discussionmentioning

confidence: 59%

Proteomic analyses of methamphetamine (METH)-induced differential protein expression by immature dendritic cells (IDC)

Reynolds

Mahajan

Sykes

et al. 2007

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

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In the US, the increase in methamphetamine (METH) use has been associated with increased human immunodeficiency virus (HIV-1) infection. Dendritic cells (DC) are the first line of defense against HIV-1. DC play a critical role in harboring HIV-1 and facilitate the infection of neighboring T cells. However, the role of METH on HIV-1 infectivity and the expression of the proteome of immature dendritic cells (IDC) has not been elucidated. We hypothesize that METH modulates the expression of a number of proteins by IDC that foster the immunopathogenesis of HIV-1 infection. We utilized LTR amplification, p24 antigen assay and the proteomic method of difference gel electrophoresis (DIGE) combined with protein identification through high performance liquid chromatographytandem mass spectrometry (HPLC-MS/MS) to analyze the effects of METH on HIV-1 infectivity (HIV-1 IIIB; CXCR4-tropic, X4 strain) and the proteomic profile of IDC. Our results demonstrate that METH potentiates HIV-1 replication in IDC. Furthermore, METH significantly differentially regulates the expression of several proteins including CXCR3, protein disulfide isomerase, procathepsin B, peroxiredoxin and galectin-1. Identification of unique, METH-induced proteins may help to develop novel markers for diagnostic, preventive and therapeutic targeting in METH using subjects.

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“…The activation of kappa-opioid receptors by cocaine is somehow involved in potentiation of HIV-1 expression and facilitation of HIV-1 associated dementia (313). Similarly, the RT-PCR analysis demonstrated the constitutive expression of mu-opioid receptor mRNA in human microglia.…”

Section: Opioid Receptorsmentioning

confidence: 92%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,134

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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κ-Opioid Receptor Ligands Inhibit Cocaine-Induced HIV-1 Expression in Microglial Cells

Cited by 39 publications

References 38 publications

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

Proteomic analyses of methamphetamine (METH)-induced differential protein expression by immature dendritic cells (IDC)

Physiology of Microglia

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