ArticleJournal of neurotrauma2014
Temporal and spatial dynamics of nrf2-antioxidant response elements mediated gene targets in cortex and hippocampus after controlled cortical impact traumatic brain injury in mice.
Article in Journal of neurotrauma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Notoginsenoside R1 Attenuates Oxidative Damage After Intracerebral Hemorrhage by Inhibiting LCN2 and Promoting HO-1 in Astrocytes.Brain sciences · 2026Article
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- The Cerebral Protective Effect of Novel Erinacines fromAntioxidants (Basel, Switzerland) · 2024Article
- Repurposing dimethyl fumarate as an antiepileptogenic and disease-modifying treatment for drug-resistant epilepsy.Journal of translational medicine · 2023Article
- Injury-Transplantation Interval-Dependent Amelioration of Axonal Degeneration and Motor Deficit in Rats with Penetrating Traumatic Brain Injury.Neurotrauma reports · 2023Article
- The NRF2-Dependent Transcriptional Regulation of Antioxidant Defense Pathways: Relevance for Cell Type-Specific Vulnerability to Neurodegeneration and Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury.International journal of molecular sciences · 2021Article
- Ketogenic regimens for acute neurotraumatic events.Current opinion in biotechnology · 2021Review
- Deficiency of Nrf2 exacerbates white matter damage and microglia/macrophage levels in a mouse model of vascular cognitive impairment.Journal of neuroinflammation · 2020Article
- Repetitive Mild Traumatic Brain Injury and Transcription Factor Modulation.Journal of neurotrauma · 2020Article
- Transcriptional activation of antioxidant gene expression by Nrf2 protects against mitochondrial dysfunction and neuronal death associated with acute and chronic neurodegeneration.Experimental neurology · 2020Review
- Traumatic brain injury-induced downregulation of Nrf2 activates inflammatory response and apoptotic cell death.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration.Journal of neurotrauma · 2019Article
- Hypocretin Mediates Sleep and Wake Disturbances in a Mouse Model of Traumatic Brain Injury.Journal of neurotrauma · 2019Article
- CD28 Deficiency Ameliorates Thoracic Blast Exposure-Induced Oxidative Stress and Apoptosis in the Brain through the PI3K/Nrf2/Keap1 Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- Chronic traumatic encephalopathy-integration of canonical traumatic brain injury secondary injury mechanisms with tau pathology.Progress in neurobiology · 2017Review
- Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Phenelzine Protects Brain Mitochondrial Function In Vitro and In Vivo following Traumatic Brain Injury by Scavenging the Reactive Carbonyls 4-Hydroxynonenal and Acrolein Leading to Cortical Histological Neuroprotection.Journal of neurotrauma · 2017Article
- Ursolic Acid Ameliorates Early Brain Injury After Experimental Traumatic Brain Injury in Mice by Activating the Nrf2 Pathway.Neurochemical research · 2017Article
- Hypocretinergic and cholinergic contributions to sleep-wake disturbances in a mouse model of traumatic brain injury.Neurobiology of sleep and circadian rhythms · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The pathophysiological importance of oxidative damage after traumatic brain injury (TBI) has been extensively demonstrated. The transcription factor nuclear factor erythoid related factor 2 (Nrf2) mediates antioxidant and cytoprotective genes by binding to antioxidant response elements (ARE) present in nuclear DNA. In this study, we characterized the time course of Nrf2-ARE-mediated expression in the cortex and hippocampus using a unilateral controlled cortical impact model of focal TBI. Ipsilateral hippocampal and cortical tissue was collected for Western-blot protein analysis (n=6/group) or quantitative reverse transcription-polymerase chain reaction for mRNA (n=3/group) at 3, 6, 12, 24, 48, and 72 h or 1 week post-injury. Multiple genes mediated by Nrf2-ARE were altered post-TBI. Specifically, Nrf2 mRNA increased significantly post-TBI at 48 and 72 h in the cortex and at 48 and 72 h and 1 week in the hippocampus with a coincident increase in glial fibrillary acidic protein mRNA, thereby implying this response is likely occurring in astrocytes. Presumably linked to Nrf2 activation, heme-oxygenase-1, nicotinamide adenine dinucleotide phosphate-quinone-oxidoreductase 1, glutathione reductase, and catalase mRNA overlap throughout the post-injury time course. This study demonstrates the first evidence of such changes during the first week after focal TBI and that increases in expression of some Nrf2-ARE-mediated cytoprotective genes are not observed until 24-48 h post-injury. Unfortunately, this does not precede, but rather coincides with, the occurrence of lipid peroxidative damage. This is the first known comparison between the time course of peroxidative damage and that of Nrf2-ARE activation during the first week post-TBI. These results underscore the necessity to discover pharmacological agents to accelerate and amplify Nrf2-ARE-mediated expression early post-TBI.
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