ArticleJournal of neurovirology2011
PTEN gene silencing prevents HIV-1 gp120(IIIB)-induced degeneration of striatal neurons.
Article in Journal of neurovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Circulating plasma protein biomarkers associated with risk of negative clinical outcomes in virally suppressed people with HIV receiving medications for opioid use disorder.Frontiers in molecular biosciences · 2026Article
- Article
- Differential Contribution of HIV-1 Subtypes B and C to Neurological Disorders: Mechanisms and Possible Treatments.AIDS reviews · 2019Review
- Exosomal miR-9 Released from HIV Tat Stimulated Astrocytes Mediates Microglial Migration.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Article
- Article
- GSK3β-activation is a point of convergence for HIV-1 and opiate-mediated interactive neurotoxicity.Molecular and cellular neurosciences · 2015Article
- Novel neuroprotective GSK-3β inhibitor restricts Tat-mediated HIV-1 replication.Journal of virology · 2014Article
- A neuroprotective phase precedes striatal degeneration upon nucleolar stress.Cell death and differentiation · 2013Article
- Exosomes derived from HIV-1-infected cells contain trans-activation response element RNA.The Journal of biological chemistry · 2013Article
- Morphine and gp120 toxic interactions in striatal neurons are dependent on HIV-1 strain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Article
- Opiate drug use and the pathophysiology of neuroAIDS.Current HIV research · 2012Review
- Fractalkine/CX3CL1 protects striatal neurons from synergistic morphine and HIV-1 Tat-induced dendritic losses and death.Molecular neurodegeneration · 2011Article
- HIV-1 envelope protein gp120 up regulates CCL5 production in astrocytes which can be circumvented by inhibitors of NF-κB pathway.Biochemical and biophysical research communications · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
To assess the role of the phosphatase and tensin homologue on chromosome 10 (PTEN) in mediating envelope glycoprotein 120 (gp120)-induced neurotoxicity in the striatum, PTEN was silenced using short interfering RNA (siRNA) vectors. PTEN activity directs multiple downstream pathways implicated in gp120-induced neuronal injury and death. PTEN is a negative regulator of Akt (protein kinase B) phosphorylation, but has also been shown to directly activate extrasynaptic NMDA receptors and dephosphorylate focal adhesion kinase. Rodent striatal neurons were nucleofected with green fluorescent protein (GFP)-expressing siRNA constructs to silence PTEN (PTENsi-GFP) or with negative-control (NCsi-GFP) vectors, and exposed to HIV-1 gp120(IIIB) using rigorously controlled, cell culture conditions including computerized time-lapse microscopy to track the fate of individual neurons following gp120 exposure. Immunofluorescence labeling showed that subpopulations of striatal neurons possess CXCR4 and CCR5 co-receptor immunoreactivity and that gp120(IIIB) was intrinsically neurotoxic to isolated striatal neurons. Importantly, PTENsi-GFP, but not control NCsi-GFP, constructs markedly decreased PTEN mRNA and protein levels and significantly attenuated gp120-induced death. These findings implicate PTEN as a critical factor in mediating the direct neurotoxic effects of HIV-1 gp120, and suggest that effectors downstream of PTEN such as Akt or other targets are potentially affected. The selective abatement of PTEN activity in neurons may represent a potential therapeutic strategy for the CNS complications of HIV-1.
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Registered trials
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