ArticleThe European journal of neuroscience2004
Preferential vulnerability of astroglia and glial precursors to combined opioid and HIV-1 Tat exposure in vitro.
Article in The European journal of neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 71 citations in OpenAlex.
- The single-cell opioid responses in the context of HIV (SCORCH) consortium.Molecular psychiatry · 2024Article
- Insufficient autophagy enables the nuclear factor erythroid 2-related factor 2 (NRF2) to promote ferroptosis in morphine-treated SH-SY5Y cells.Psychopharmacology · 2024Article
- Opioid and neuroHIV Comorbidity - Current and Future Perspectives.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Opiate Drugs with Abuse Liability Hijack the Endogenous Opioid System to Disrupt Neuronal and Glial Maturation in the Central Nervous System.Frontiers in pediatrics · 2017Review
- Chronic distress and the vulnerable host: a new target for HIV treatment and prevention?Neurobehavioral HIV medicine · 2016Article
- Chronic SIV and morphine treatment increases heat shock protein 5 expression at the synapse.Journal of neurovirology · 2015Article
- Acupuncture at Baihui and Dazhui reduces brain cell apoptosis in heroin readdicts.Neural regeneration research · 2014Article
- Opiate addiction therapies and HIV-1 Tat: interactive effects on glial [Ca²⁺]i, oxyradical and neuroinflammatory chemokine production and correlative neurotoxicity.Current HIV research · 2014Article
- Novel neuroprotective GSK-3β inhibitor restricts Tat-mediated HIV-1 replication.Journal of virology · 2014Article
- Interactions of HIV and drugs of abuse: the importance of glia, neural progenitors, and host genetic factors.International review of neurobiology · 2014Review
- HIV and recent illicit drug use interact to affect verbal memory in women.Journal of acquired immune deficiency syndromes (1999) · 2013Article
- A Bivalent Ligand Targeting the Putative Mu Opioid Receptor and Chemokine Receptor CCR5 Heterodimers: Binding Affinity versus Functional Activities.MedChemComm · 2013Article
- Transcriptome sequencing of gene expression in the brain of the HIV-1 transgenic rat.PloS one · 2013Article
- Article
- Opiate drug use and the pathophysiology of neuroAIDS.Current HIV research · 2012Review
- Cocaine and HIV-1 interplay in CNS: cellular and molecular mechanisms.Current HIV research · 2012Review
- Immunomodulatory properties of kappa opioids and synthetic cannabinoids in HIV-1 neuropathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- Methamphetamine and HIV-1 Tat down regulate β-catenin signaling: implications for methampetamine abuse and HIV-1 co-morbidity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Article
- A failure to normalize biochemical and metabolic insults during morphine withdrawal disrupts synaptic repair in mice transgenic for HIV-gp120.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Article
- Exploring the neuroimmunopharmacology of opioids: an integrative review of mechanisms of central immune signaling and their implications for opioid analgesia.Pharmacological reviews · 2011Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus (HIV)-1 infection can cause characteristic neural defects such as progressive motor dysfunction, striatal pathology and gliosis. Recent evidence suggests that HIV-induced pathogenesis is exacerbated by heroin abuse and that the synergistic neurotoxicity is a direct effect of heroin on the CNS, an alarming observation considering the high incidence of HIV infection with injection drug abuse. Although HIV infection results in neurodegeneration, neurons themselves are not directly infected. Instead, HIV affects microglia and astroglia, which subsequently contributes to the neurodegenerative changes. Opioid receptors are widely expressed by macroglia and macroglial precursors, and the activation of mu-opioid receptors can modulate programmed cell death, as well as the response of neural cells to cytotoxic insults. For this reason, we questioned whether opioid drugs might modify the vulnerability of macroglia and macroglial precursors to HIV-1 Tat protein. To address this problem, the effects of morphine and/or HIV Tat(1-72) on the viability of macroglia and macroglial precursors were assessed in mixed-glial cultures derived from mouse striatum. Our findings indicate that sustained exposure to morphine and Tat(1-72) viral protein induces the preferential death of glial precursors and some astrocytes. Moreover, the increased cell death is mediated by mu-opioid receptors and accompanied by the activation of caspase-3. Our results imply that opiates can enhance the cytotoxicity of HIV-1 Tat through direct actions on glial precursors and/or astroglia, suggesting novel cellular targets for HIV-opiate interactions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.