ArticleExperimental neurology2009
Neuronal survival and resistance to HIV-1 Tat toxicity in the primary culture of rat fetal neurons.
Article in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Suppression of HIV-TAT and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters.Journal of neurovirology · 2024Article
- Suppression of HIV and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters.bioRxiv : the preprint server for biology · 2023Article
- Inhibition of the Dead Box RNA Helicase 3 Prevents HIV-1 Tat and Cocaine-Induced Neurotoxicity by Targeting Microglia Activation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Article
- HIV-1 Tat: Role in Bystander Toxicity.Frontiers in cellular and infection microbiology · 2020Review
- HIV Infection Induces Extracellular Cathepsin B Uptake and Damage to Neurons.Scientific reports · 2019Article
- Network analysis of hippocampal neurons by microelectrode array in the presence of HIV-1 Tat and cocaine.Journal of cellular physiology · 2018Article
- Human Immunodeficiency Virus Type 1 gp120 and Tat Induce Mitochondrial Fragmentation and Incomplete Mitophagy in Human Neurons.Journal of virology · 2018Article
- Human Immunodeficiency Virus Promotes Mitochondrial Toxicity.Neurotoxicity research · 2017Review
- HIV, Tat and dopamine transmission.Neurobiology of disease · 2017Review
- HIV-1 Tat and cocaine mediated synaptopathy in cortical and midbrain neurons is prevented by the isoflavone Equol.Frontiers in microbiology · 2015Article
- Anti-tat Hutat2:Fc mediated protection against tat-induced neurotoxicity and HIV-1 replication in human monocyte-derived macrophages.Journal of neuroinflammation · 2014Article
- Synaptodendritic recovery following HIV Tat exposure: neurorestoration by phytoestrogens.Journal of neurochemistry · 2014Article
- HIV-1 Tat protein variants: critical role for the cysteine region in synaptodendritic injury.Experimental neurology · 2013Article
- Human immunodeficiency virus-1 protein Tat induces excitotoxic loss of presynaptic terminals in hippocampal cultures.Molecular and cellular neurosciences · 2013Article
- D1/NMDA receptors and concurrent methamphetamine+ HIV-1 Tat neurotoxicity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Article
- Article
- Oxygen matters: tissue culture oxygen levels affect mitochondrial function and structure as well as responses to HIV viroproteins.Cell death & disease · 2011Article
- Morphine potentiates neurodegenerative effects of HIV-1 Tat through actions at μ-opioid receptor-expressing glia.Brain : a journal of neurology · 2011Article
- ER-β mediates 17β-estradiol attenuation of HIV-1 Tat-induced apoptotic signaling.Synapse (New York, N.Y.) · 2010Article
- E2F1 localizes predominantly to neuronal cytoplasm and fails to induce expression of its transcriptional targets in human immunodeficiency virus-induced neuronal damage.Neuroscience letters · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In this study we report that primary cultures of rat fetal neurons contain subpopulations of cells that may be sensitive or resistant to HIV-1 Tat neurotoxicity. We demonstrate that rapid binding/uptake of Tat 1-86 for 2 h was sufficient to trigger caspase activation and neurodegeneration in rat fetal midbrain cell cultures. The uptake of Tat was followed by an increase in MCP1 (CCL2) immunoreactivity. Approximately 70% of neurons were able to survive transient or continuous (7 days) Tat exposure. The surviving neurons did not contain bound/internalized Tat, but were able to interact with Tat after medium replacement. These neurons were resistant to Tat toxicity. In neurons that resisted the toxic effects of continuous and repeated Tat treatment, levels of NR2A subunit of the NMDA receptor complex were significantly lower than in controls. We suggest that the subunit composition of NMDAR complexes may be important for the sensitivity of neurons to Tat toxicity.
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Registered trials
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.