ArticleTranslational stroke research2010
Ischemic preconditioning mediates cyclooxygenase-2 expression via nuclear factor-kappa B activation in mixed cortical neuronal cultures.
Article in Translational stroke research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Alcohol Dependence Modulates Amygdalar mTORC2 and PKCε Expression in a Rodent Model.Nutrients · 2023Article
- Research progress of mitophagy in chronic cerebral ischemia.Frontiers in aging neuroscience · 2023Review
- Neuroprotective effects and mechanisms of ischemic/hypoxic preconditioning on neurological diseases.CNS neuroscience & therapeutics · 2021Review
- Ischemic Neuroprotectant PKCε Restores Mitochondrial Glutamate Oxaloacetate Transaminase in the Neuronal NADH Shuttle after Ischemic Injury.Translational stroke research · 2020Article
- Preactivation of Notch1 in remote ischemic preconditioning reduces cerebral ischemia-reperfusion injury through crosstalk with the NF-κB pathway.Journal of neuroinflammation · 2019Article
- Estrogen preconditioning: A promising strategy to reduce inflammation in the ischemic brain.Conditioning medicine · 2019Article
- Mitochondrial Dysfunction in Neural Injury.Frontiers in neuroscience · 2019Review
- Vinpocetine Inhibits NF-κB-Dependent Inflammation in Acute Ischemic Stroke Patients.Translational stroke research · 2018Article
- Ischemic Preconditioning Protects Astrocytes against Oxygen Glucose Deprivation Via the Nuclear Erythroid 2-Related Factor 2 Pathway.Translational stroke research · 2018Article
- (-)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury.Brain research · 2017Article
- Ischemic preconditioning treatment of astrocytes transfers ischemic tolerance to neurons.Conditioning medicine · 2017Article
- Roles of HIF-1α, VEGF, and NF-κB in Ischemic Preconditioning-Mediated Neuroprotection of Hippocampal CA1 Pyramidal Neurons Against a Subsequent Transient Cerebral Ischemia.Molecular neurobiology · 2017Article
- Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease.Frontiers in molecular neuroscience · 2016Review
- Rational modulation of the innate immune system for neuroprotection in ischemic stroke.Frontiers in neuroscience · 2015Review
- Oxidative Stress and the Use of Antioxidants in Stroke.Antioxidants (Basel, Switzerland) · 2014Review
- Non-pharmaceutical therapies for stroke: mechanisms and clinical implications.Progress in neurobiology · 2014Review
- Article
- Sunitinib enhances neuronal survival in vitro via NF-κB-mediated signaling and expression of cyclooxygenase-2 and inducible nitric oxide synthase.Journal of neuroinflammation · 2013Article
- Apobec-1 increases cyclooxygenase-2 and aggravates injury in oxygen-deprived neurogenic cells and middle cerebral artery occlusion rats.Neurochemical research · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear factor-kappaB (NF-κB) activation occurs following ischemic preconditioning (IPC) in brain. However, the upstream signaling messengers and down-stream targets of NF-κB required for induction of IPC remain undefined. In a previous study, we demonstrated that epsilon protein kinase c (εPKC) was a key mediator of IPC in brain. Activation of εPKC induced cyclooygenase-2 (COX-2) expression and conferred ischemic tolerance in the neuronal and hippocampal slice models. Here, we hypothesized that IPC-mediated COX-2 expression was mediated by NF-κB. We tested this hypothesis in mixed cortical neuron/astrocyte cell cultures. To simulate IPC or ischemia, cell cultures were exposed to 1 or 4 h of oxygen-glucose deprivation, respectively. Our results demonstrated translocation of p65 and p50 subunits of NF-κB into nucleus following IPC or εPKC activation. NF-κB inhibition with pyrrolidine dithiocarbamate (10 μM) abolished IPC or εPKC activator-mediated neuroprotection indicating that NF-κB activation was involved in ischemic tolerance. In parallel studies, inhibition of either εPKC or the extracellular signal-regulated kinase (ERK 1/2) pathway reduced IPC-induced NF-κB activation. Finally, inhibition of NF-κB blocked IPC-induced COX-2 expression. In conclusion, we demonstrated that IPC-signaling cascade comprises εPKC activation→ERK1/2 activation→NF-κB translocation to nucleus→COX-2 expression resulting in neuroprotection in mixed neuronal culture.
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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.