ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2011
HIV-1 gp120-induced axonal injury detected by accumulation of β-amyloid precursor protein in adult rat corpus callosum.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Alzheimer's-Like Pathology at the Crossroads of HIV-Associated Neurological Disorders.Vaccines · 2021Review
- HIV Infection and Related Mental Disorders.Brain sciences · 2021Review
- Blood amyloid-β protein isoforms are affected by HIV-1 in a subtype-dependent pattern.Journal of neurovirology · 2020Article
- Cross-talk between microglia and neurons regulates HIV latency.PLoS pathogens · 2019Article
- A Case of HIV Seroconversion Presenting Similarly to Anti-N-methyl-D-aspartate Receptor Encephalitis.Neurocritical care · 2019Article
- Does HIV infection contribute to increased beta-amyloid synthesis and plaque formation leading to neurodegeneration and Alzheimer's disease?Journal of neurovirology · 2019Review
- Severer nodular lesion in white matter than in gray matter in simian immunodeficiency virus-infected monkey, but not closely correlated with viral infection.Journal of biomedical research · 2019Article
- Extracellular Vesicles: A Possible Link between HIV and Alzheimer's Disease-Like Pathology in HIV Subjects?Cells · 2019Review
- "APP"reciating the complexity of HIV-induced neurodegenerative diseases.PLoS pathogens · 2018Article
- Neprilysin in the Cerebrospinal Fluid and Serum of Patients Infected With HIV1-Subtypes C and B.Journal of acquired immune deficiency syndromes (1999) · 2018Article
- Biomarkers of neuronal injury and amyloid metabolism in the cerebrospinal fluid of patients infected with HIV-1 subtypes B and C.Journal of neurovirology · 2018Article
- The alpha7-nicotinic receptor contributes to gp120-induced neurotoxicity: implications in HIV-associated neurocognitive disorders.Scientific reports · 2018Article
- Article
- The lipid raft-dwelling protein US9 can be manipulated to target APP compartmentalization, APP processing, and neurodegenerative disease pathogenesis.Scientific reports · 2017Article
- HIV-1 Glycoprotein 120 Enhancement of N-Methyl-D-Aspartate NMDA Receptor-Mediated Excitatory Postsynaptic Currents: Implications for HIV-1-Associated Neural Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- The Role of HIV Infection in Neurologic Injury.Brain sciences · 2017Review
- HIV-1 Transactivator Protein Induces ZO-1 and Neprilysin Dysfunction in Brain Endothelial Cells via the Ras Signaling Pathway.Oxidative medicine and cellular longevity · 2017Article
- An Overview of Human Immunodeficiency Virus Type 1-Associated Common Neurological Complications: Does Aging Pose a Challenge?Journal of Alzheimer's disease : JAD · 2017Review
- Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders.Brain sciences · 2016Review
- EXPRESS: Oligodendrocytes in HIV-associated pain pathogenesis.Molecular pain · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 brain infection induces neurodegeneration. While most studies focus on HIV-1-mediated neuronal injury, relatively few have investigated HIV-1-associated white matter damage. Corpus callosum (CC) is one of frequently involved white matter structures in HIV-1-associated white matter damage. Utilizing a model of ex vivo treatment of brain slice containing CC with HIV-1 glycoprotein 120 (gp120), we examined axonal injury by analyzing β-amyloid precursor protein (β-APP) accumulation in the axon. Incubation of CC slice with gp120 produced a significant higher density of β-APP in the CC tissue compared with non-gp120-treated controls, suggesting the presence of axonal damage in the CC. The gp120-induced CC axonal damage was blocked by a chemokine CXCR4 receptor antagonist T140 but not by an NMDA receptor blocker MK801 as demonstrated by Western blot analysis of β-APP, indicating that gp120 evokes the CC axonal injury through CXCR4 receptor. Immunocytochemical studies revealed a surprisingly high density of CXCR4-positive immunoreactivity in the CC. The CXCR4-positive labeling was distributed along the nerve fibers. Moreover, double labeling of anti-CXCR4 with either anti-neuronal nuclei or anti-myelin/oligodendrocyte-specific protein antibody revealed co-localization of CXCR4 and myelin/oligodendrocytes in some fiber-like structures, inferring that some neurons and oligodendrocytes in the CC express CXCR4. Taken together, these results indicate that gp120 induced axonal damage via CXCR4 in the CC.
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