ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Activation of p38 MAPK is required in monocytic and neuronal cells for HIV glycoprotein 120-induced neurotoxicity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 81 citations in OpenAlex.
- HIV Infection, Neurotoxicity, Inflammation, Premature Aging, and Therapeutic Challenges to PLWH: An Overview.International journal of molecular sciences · 2026Review
- EphB2-mediated ephrin-B reverse signaling on microglia drives an anti-viral, but inflammatory and neurotoxic response associated with HIV.Journal of neuroinflammation · 2025Article
- Human Stress Response Specificity through Bioresonance Selectivity.bioRxiv : the preprint server for biology · 2025Article
- Nanopathways modulating postoperative cognitive dysfunction: extracellular vesicles.Frontiers in cell and developmental biology · 2025Review
- Modulating neuroinflammation and cognitive function in postoperative cognitive dysfunction via CCR5-GPCRs-Ras-MAPK pathway targeting with microglial EVs.CNS neuroscience & therapeutics · 2024Article
- A critical role for Macrophage-derived Cysteinyl-Leukotrienes in HIV-1 induced neuronal injury.Brain, behavior, and immunity · 2024Article
- Interferon-β deficiency alters brain response to chronic HIV-1 envelope protein exposure in a transgenic model of NeuroHIV.Brain, behavior, and immunity · 2024Article
- HIV-Associated Dementia: Associated Factors and Characteristics of Cognitive Domain Abnormalities in Elderly People Living with HIV Treated with Highly Active Antiretroviral Therapy.The American journal of tropical medicine and hygiene · 2022Article
- HIV-Proteins-Associated CNS Neurotoxicity, Their Mediators, and Alternative Treatments.Cellular and molecular neurobiology · 2022Review
- Article
- HIV and FIV glycoproteins increase cellular tau pathology via cGMP-dependent kinase II activation.Journal of cell science · 2022Article
- Review
- Advances in the Experimental Models of HIV-Associated Neurological Disorders.Current HIV/AIDS reports · 2021Review
- Review
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Beneficial and Adverse Effects of cART Affect Neurocognitive Function in HIV-1 Infection: Balancing Viral Suppression against Neuronal Stress and Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- Transcriptomic and Genetic Profiling of HIV-Associated Neurocognitive Disorders.Frontiers in molecular biosciences · 2021Review
- Engagement of Neurotropic Viruses in Fast Axonal Transport: Mechanisms, Potential Role of Host Kinases and Implications for Neuronal Dysfunction.Frontiers in cellular neuroscience · 2021Article
- Lipocalin-2 mediates HIV-1 induced neuronal injury and behavioral deficits by overriding CCR5-dependent protection.Brain, behavior, and immunity · 2020Article
- A pivotal role for Interferon-α receptor-1 in neuronal injury induced by HIV-1.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
HIV-1 envelope protein gp120 has been implicated in neurotoxin production by monocytic cells (i.e., macrophages and microglia), as well as in the pathogenesis of HIV-1-associated neurocognitive disorders. We previously showed in cerebrocortical cell cultures from rodents containing microglia, astrocytes, and neurons that overall inhibition of p38 MAPK signaling abrogated the neurotoxic effect of HIV-1 gp120. However, the time course of p38 MAPK activation and the contribution of this kinase in the various cell types remained unknown. In this study, we found that active p38 MAPK is required in monocytic lineage cells (i.e., macrophages and microglia) and neuronal cells for HIV gp120-induced neurotoxicity to occur. In cerebrocortical cell cultures, HIV-1 gp120 stimulated a time-dependent overall increase in active p38 MAPK, and the activated kinase was primarily detected in microglia and neurons. Interestingly, increased activation of p38 MAPK and neuronal death in response to gp120 were prevented by prior depletion of microglia or the presence of CCR5 ligand CCL4 or p38 MAPK inhibitors. In human monocytic THP-1 cells and primary monocyte-derived macrophages, HIV gp120-stimulated production of neurotoxins was abrogated by prior introduction into the cells of a dominant-negative p38 MAPK mutant or p38 MAPK small interfering RNA. In addition, the neurotoxic effects of cell-free supernatants from gp120-stimulated monocytic THP-1 cells were prevented in microglia-depleted cerebrocortical cells pretreated with a pharmacological inhibitor of p38 MAPK. Thus, p38 MAPK signaling was critical, upon exposure to HIV gp120, for the neurotoxic phenotype of monocytic cells and subsequent toxin-initiated neuronal apoptosis.
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