ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Essential role for zinc-triggered p75NTR activation in preconditioning neuroprotection.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- An increase of lysosomes through EGF-triggered endocytosis attenuated zinc-mediated lysosomal membrane permeabilization and neuronal cell death.Cell death & disease · 2024Article
- The Function and Regulation of Zinc in the Brain.Neuroscience · 2021Review
- Zinc Transporter-3 Knockout Mice Demonstrate Age-Dependent Alterations in the Metalloproteome.International journal of molecular sciences · 2020Article
- Mechanism of Zinc Excitotoxicity: A Focus on AMPK.Frontiers in neuroscience · 2020Review
- Zinc Signal in Brain Diseases.International journal of molecular sciences · 2017Review
- Zinc wave during the treatment of hypoxia is required for initial reactive oxygen species activation in mitochondria.International journal of physiology, pathophysiology and pharmacology · 2016Article
- Poly(ADP-ribosyl)ation of p53 contributes to TPEN-induced neuronal apoptosis.Molecules and cells · 2015Article
- Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia.Neural plasticity · 2015Article
- Subacute zinc administration and L-NAME caused an increase of NO, zinc, lipoperoxidation, and caspase-3 during a cerebral hypoxia-ischemia process in the rat.Oxidative medicine and cellular longevity · 2013Article
- Zinc induces long-term upregulation of T-type calcium current in hippocampal neurons in vivo.The Journal of physiology · 2012Article
- Redox regulation of intracellular zinc: molecular signaling in the life and death of neurons.Antioxidants & redox signaling · 2011Review
- Zinc: new clues to diverse roles in brain ischemia.Trends in pharmacological sciences · 2011Review
- The relationship between transient zinc ion fluctuations and redox signaling in the pathways of secondary cellular injury: relevance to traumatic brain injury.Brain research · 2010Article
- Cognitive loss in zinc transporter-3 knock-out mice: a phenocopy for the synaptic and memory deficits of Alzheimer's disease?The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Zn2+ regulates Kv2.1 voltage-dependent gating and localization following ischemia.The European journal of neuroscience · 2009Article
- Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning.Journal of neurochemistry · 2009Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic preconditioning (PC) of the brain is a phenomenon by which mild ischemic insults render neurons resistant to subsequent strong insults. Key steps in ischemic PC of the brain include caspase-3 activation and poly(ADP-ribose) polymerase-1 (PARP-1) cleavage, but upstream events have not been clearly elucidated. We have tested whether endogenous zinc is required for ischemic PC of the brain in rats. Mild, transient zinc accumulation was observed in certain neurons after ischemic PC. Moreover, intraventricular administration of CaEDTA during ischemic PC abrogated both zinc accumulation and the protective effect against subsequent full ischemia. To elucidate the mechanism of the zinc-triggered PC (Zn PC) effect, cortical cultures were exposed to sublethal levels of zinc, and 18 h later to lethal levels of zinc or NMDA. Zn PC exhibited the characteristic features of ischemic PC, including caspase-3 activation, PARP-1 cleavage, and HSP70 induction, all of which are crucial for subsequent neuroprotection against NMDA or zinc toxicity. HSP70 induction was necessary for protection, as it halted caspase-3 activation before apoptosis. Interestingly, in both Zn PC in vitro and ischemic PC in vivo, p75(NTR) was necessary for neuroprotection. These results suggest that caspase-3 activation during ischemic PC, a necessary event for subsequent neuroprotection, may result from mild zinc accumulation and the consequent p75(NTR) activation in neurons.
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