ArticlePloS one2013
Chemokine co-receptor CCR5/CXCR4-dependent modulation of Kv2.1 channel confers acute neuroprotection to HIV-1 glycoprotein gp120 exposure.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- An in-depth exploration of snake venom-derived molecules for drug discovery in advancing antiviral therapeutics.Heliyon · 2024Review
- Sensory neuron dysfunction in orthotopic mouse models of colon cancer.Journal of neuroinflammation · 2022Article
- Review
- CCR5 closes the temporal window for memory linking.Nature · 2022Article
- Recent Advances in the Molecular and Cellular Mechanisms of gp120-Mediated Neurotoxicity.Cells · 2022Review
- New research tools suggest a "levels-less" image of the behaving organism and dissolution of the reduction vs. anti-reduction dispute.Frontiers in psychology · 2022Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Discovery of HIV entry inhibitors via a hybrid CXCR4 and CCR5 receptor pharmacophore-based virtual screening approach.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Linked CSF reduction of phosphorylated tau and IL-8 in HIV associated neurocognitive disorder.Scientific reports · 2019Article
- CCR5/CXCR4 Dual Antagonism for the Improvement of HIV Infection Therapy.Molecules (Basel, Switzerland) · 2019Review
- Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability.Oncology letters · 2018Article
- Angiotensin II Triggers Peripheral Macrophage-to-Sensory Neuron Redox Crosstalk to Elicit Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- HIV induces synaptic hyperexcitation via cGMP-dependent protein kinase II activation in the FIV infection model.PLoS biology · 2018Article
- Disruption of KNeuroscience · 2017Article
- Zn(2+) -induced Ca(2+) release via ryanodine receptors triggers calcineurin-dependent redistribution of cortical neuronal Kv2.1 K(+) channels.The Journal of physiology · 2016Article
- HIV-1 gp120Bal down-Regulates Phosphorylated NMDA Receptor Subunit 1 in Cortical Neurons via Activation of Glutamate and Chemokine Receptors.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Target of HIV-1 Envelope Glycoprotein gp120-Induced Hippocampal Neuron Damage: Role of Voltage-Gated K(+) Channel Kv2.1.Viral immunology · 2015Article
- Article
- Cyclin e1 regulates Kv2.1 channel phosphorylation and localization in neuronal ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Infection with human immunodeficiency virus-1 (HIV-1) within the brain has long been known to be associated with neurodegeneration and neurocognitive disorder (referred as HAND), a condition characterized in its early stages by declining cognitive function and behavioral disturbances. Mechanistically, the HIV-1 coat glycoprotein 120 (gp120) has been suggested to be a critical factor inducing apoptotic cell death in neurons via the activation of p38 mitogen-activated protein kinase (MAPK), upon chronic exposure to the virus. Here we show that acute exposure of neurons to HIV-1 gp120 elicits a homeostatic response, which provides protection against non-apoptotic cell death, involving the major somatodendritic voltage-gated K⁺ (Kv) channel Kv2.1 as the key mediator. The Kv2.1 channel has recently been shown to provide homeostatic control of neuronal excitability under conditions of seizures, ischemia and neuromodulation/neuroinflammation. Following acute exposure to gp120, cultured rat hippocampal neurons show rapid dephosphorylation of the Kv2.1 protein, which ultimately leads to changes in specific sub-cellular localization and voltage-dependent channel activation properties of Kv2.1. Such modifications in Kv2.1 are dependent on the activation of the chemokine co-receptors CCR5 and CXCR4, and subsequent activation of the protein phosphatase calcineurin. This leads to the overall suppression of neuronal excitability and provides neurons with a homeostatic protective mechanism. Specific blockade of calcineurin and Kv2.1 channel activity led to significant enhancement of non-apoptotic neuronal death upon acute gp120 treatment. These observations shed new light on the intrinsic homeostatic mechanisms of neuronal resilience during the acute stages of neuro-HIV infections.
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