ArticleJournal of molecular neuroscience : MN2014
PACAP27 is protective against tat-induced neurotoxicity.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Oxidative phosphorylation in HIV-1 infection: impacts on cellular metabolism and immune function.Frontiers in immunology · 2024Review
- Meta-Analysis of the Mechanisms Underlying COVID-19 Modulation of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Human immunodeficiency virus and antiretroviral therapy-mediated immune cell metabolic dysregulation in children born to HIV-infected women: potential clinical implications.Frontiers in immunology · 2023Review
- Effects of Pituitary Adenylate Cyclase Activating Polypeptide on Cell Death.International journal of molecular sciences · 2022Review
- Effect of NSAIDs Supplementation on the PACAP-, SP- and GAL-Immunoreactive Neurons in the Porcine Jejunum.International journal of molecular sciences · 2021Article
- HIV-1 Tat Activates Akt/mTORC1 Pathway and AICDA Expression by Downregulating Its Transcriptional Inhibitors in B Cells.International journal of molecular sciences · 2021Article
- HIV influences microtubule associated protein-2: potential marker of HIV-associated neurocognitive disorders.AIDS (London, England) · 2020Article
- The Role of Selected Pro-Inflammatory Cytokines in Pathogenesis of Ischemic Stroke.Clinical interventions in aging · 2020Review
- Human immunodeficiency virus Tat impairs mitochondrial fission in neurons.Cell death discovery · 2018Article
- Neuroprotective effects of fatty acid amide hydrolase catabolic enzyme inhibition in a HIV-1 Tat model of neuroAIDS.Neuropharmacology · 2018Article
- The orphan G-protein-coupled receptor 75 signaling is activated by the chemokine CCL5.Journal of neurochemistry · 2018Article
- Review on PACAP-Induced Transcriptomic and Proteomic Changes in Neuronal Development and Repair.International journal of molecular sciences · 2018Review
- Examining Relationships between Metabolism and Persistent Inflammation in HIV Patients on Antiretroviral Therapy.Mediators of inflammation · 2018Review
- Human Immunodeficiency Virus Promotes Mitochondrial Toxicity.Neurotoxicity research · 2017Review
- Conditional Human Immunodeficiency Virus Transactivator of Transcription Protein Expression Induces Depression-like Effects and Oxidative Stress.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2017Article
- Glial- and Neuronal-Specific Expression of CCL5 mRNA in the Rat Brain.Frontiers in neuroanatomy · 2017Article
- Identification of a binding site of the human immunodeficiency virus envelope protein gp120 to neuronal-specific tubulin.Journal of neurochemistry · 2016Article
- Analogs of the novel phytohormone, strigolactone, trigger apoptosis and synergize with PARP inhibitors by inducing DNA damage and inhibiting DNA repair.Oncotarget · 2016Article
- Pharmacological induction of CCL5 in vivo prevents gp120-mediated neuronal injury.Neuropharmacology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Human immunodeficiency virus type-1 (HIV) infection of the central nervous system promotes neuronal injury and apoptosis that culminate in HIV-associated neurocognitive disorders (HAND). Viral proteins, such as transactivator of transcription (Tat), have emerged as leading candidates to explain HIV-mediated neurotoxicity, though the mechanism remains unclear. To determine the effects of Tat, rat cortical neurons were exposed to nanomolar concentrations of Tat for various time points. Within a few hours, Tat induced the production of reactive oxygen species (ROS), and other indices of mitochondrial destabilization. In addition, we observed a significant induction of DNA double-strand breaks (DSBs) by Tat. We next investigated the neuroprotective activity of the pituitary adenylate cyclase-activating polypeptide 27 (PACAP27) against these cardinal features of Tat-induced neurodegeneration. PACAP27 (100 nM) inhibited all Tat-mediated toxic effects including DNA DSBs. Importantly, PACAP27 prevented the induction of neuronal loss induced by Tat. The neuroprotective effect of PACAP27 is correlated with its ability to release the anti-apoptotic chemokine CCL5. Our data support a mechanism of Tat neurotoxicity in which Tat induces mitochondrial destabilization, thus increasing the release of ROS, which causes DNA DSBs leading to cell death. PACAP27, through CCL5, mitigates the effects of Tat-induced neuronal dysfunction, suggesting that PACAP27 could be a new strategy for an adjunct therapy against HIV-associated neurocognitive disorders.
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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.