ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Neuroprotective effects of reactive oxygen species mediated by BDNF-independent activation of TrkB.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Cuproptosis: New Mechanisms Linking Endothelial Dysfunction to Neurodegenerative Diseases and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Depletion of placental brain-derived neurotrophic factor (BDNF) is attributed to premature ovarian insufficiency (POI) in mice offspring.Journal of ovarian research · 2024Article
- Targeting Biometals in Alzheimer's Disease with Metal Chelating Agents Including Coumarin Derivatives.CNS drugs · 2024Review
- Metal-Chelating Self-Assembling Peptide Nanofiber Scaffolds for Modulation of Neuronal Cell Behavior.Micromachines · 2023Article
- Reprogramming of adult human dermal fibroblasts to induced dorsal forebrain precursor cells maintains aging signatures.Frontiers in cellular neuroscience · 2023Article
- The Role of Metals in the Neuroregenerative Action of BDNF, GDNF, NGF and Other Neurotrophic Factors.Biomolecules · 2022Review
- Aluminium oxide nanoparticles compromise spatial memory performance and proBDNF-mediated neuronal function in the hippocampus of rats.Particle and fibre toxicology · 2022Article
- The Elusive "Switch Process" in Bipolar Disorder and Photoperiodism: A Hypothesis Centering on NADPH Oxidase-Generated Reactive Oxygen Species Within the Bed Nucleus of the Stria Terminalis.Frontiers in psychiatry · 2022Article
- Exploring Hyperoxia Effects in Cancer-From Perioperative Clinical Data to Potential Molecular Mechanisms.Biomedicines · 2021Review
- Review
- Dimeric mimetic of BDNF loop 4 promotes survival of serum-deprived cell through TrkB-dependent apoptosis suppression.Scientific reports · 2021Article
- Neuroprotective Potential of Verbascoside Isolated fromAntioxidants (Basel, Switzerland) · 2020Article
- Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment.Antioxidants (Basel, Switzerland) · 2020Review
- Article
- A NeurotoxicFrontiers in molecular neuroscience · 2020Review
- TRPM7 senses oxidative stress to release ZnProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Role of reactive oxygen species and TRP channels in the cough reflex.Cell calcium · 2016Review
- Protective Effect of Silibinin on Learning and Memory Impairment in LPS-Treated Rats via ROS-BDNF-TrkB Pathway.Neurochemical research · 2016Article
- Expression profile analysis of hippocampal CA1 pyramidal neurons in aged Ts65Dn mice, a model of Down syndrome (DS) and Alzheimer's disease (AD).Brain structure & function · 2015Article
- Increased cortical synaptic activation of TrkB and downstream signaling markers in a mouse model of Down Syndrome.Neurobiology of disease · 2015Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Reactive oxygen species (ROS) have diverse biological consequences in the mammalian CNS, but the molecular targets mediating these pleiotropic effects are incompletely understood. Like ROS, the neurotrophin receptor, TrkB receptor tyrosine kinase, has diverse effects in the developing and mature mammalian brain. Our discovery that zinc can transactivate TrkB, together with the finding that ROS can trigger zinc release from cytosolic zinc binding proteins, led us to hypothesize that ROS can transactivate TrkB in CNS neurons by a zinc-dependent mechanism. We found that both exogenous H(2)O(2) and endogenous ROS activate TrkB signaling by a Src family kinase-dependent but brain-derived neurotrophic factor-independent mechanism in cultured rat cortical neurons. Exogenous H(2)O(2) enhances cytosolic zinc content in a metallothionein-3 (MT-3)-requiring manner. Both exogenous H(2)O(2) and endogenous ROS mediated transactivation of TrkB requires intracellular zinc and MT-3. The ROS-triggered transactivation of TrkB exerts neuroprotective effects, because inhibition of TrkB kinase activity or uncoupling Shc signaling from TrkB exacerbates neuronal cell death induced by H(2)O(2). Thus, we propose a molecular signaling event whereby ROS induce release of zinc from cytosolic MT-3, the increased cytosolic zinc transactivates TrkB, and the enhanced Shc signaling downstream from TrkB promotes prosurvival effects. We suggest that such neuroprotective effects mediated by ROS are operative in diverse acute and chronic neurological disorders.
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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.