ArticleFrontiers in cellular neuroscience2014
Altering endoplasmic reticulum stress in a model of blast-induced traumatic brain injury controls cellular fate and ameliorates neuropsychiatric symptoms.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- Nandrolone Abuse Prior to Head Trauma Mitigates Endoplasmic Reticulum Stress, Mitochondrial Bioenergetic Deficits, and Markers of Neurodegeneration.Molecular neurobiology · 2025Article
- The impact of adolescent drinking on traumatic brain injury-induced cognitive deficits and alcohol preference in adult C57BL/6J mice.Alcohol, clinical & experimental research · 2025Article
- Endoplasmic reticulum stress and the unfolded protein response: emerging regulators in progression of traumatic brain injury.Cell death & disease · 2024Review
- Nervous System Response to Neurotrauma: A Narrative Review of Cerebrovascular and Cellular Changes After Neurotrauma.Journal of molecular neuroscience : MN · 2024Review
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
- Modulation of the endoplasmic reticulum stress and unfolded protein response mitigates the behavioral effects of early-life stress.Pharmacological reports : PR · 2023Article
- Oxidative stress in the brain and retina after traumatic injury.Frontiers in neuroscience · 2023Review
- Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer's disease, and epilepsy.Frontiers in neurology · 2023Article
- Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway.Brain and behavior · 2022Article
- Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence.Diseases (Basel, Switzerland) · 2022Review
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Synergistic effects of brain injury and aging: common mechanisms of proteostatic dysfunction.Trends in neurosciences · 2021Review
- Blast-induced temporal alterations in blood-brain barrier properties in a rodent model.Scientific reports · 2021Article
- Activation of the Protein Kinase R-Like Endoplasmic Reticulum Kinase (PERK) Pathway of the Unfolded Protein Response after Experimental Traumatic Brain Injury and Treatment with a PERK Inhibitor.Neurotrauma reports · 2021Article
- Endoplasmic Reticulum Stress-Associated Neuronal Death and Innate Immune Response in Neurological Diseases.Frontiers in immunology · 2021Review
- Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents.Journal of visualized experiments : JoVE · 2020Article
- Nitric oxide synthase mediates cerebellar dysfunction in mice exposed to repetitive blast-induced mild traumatic brain injury.Scientific reports · 2020Article
- Salubrinal enhances eIF2α phosphorylation and improves fertility in a mouse model of Classic Galactosemia.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria.Neural regeneration research · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal injury following blast-induced traumatic brain injury (bTBI) increases the risk for neuropsychiatric disorders, yet the pathophysiology remains poorly understood. Blood-brain-barrier (BBB) disruption, endoplasmic reticulum (ER) stress, and apoptosis have all been implicated in bTBI. Microvessel compromise is a primary effect of bTBI and is postulated to cause subcellular secondary effects such as ER stress. What remains unclear is how these secondary effects progress to personality disorders in humans exposed to head trauma. To investigate this we exposed male rats to a clinically relevant bTBI model we have recently developed. The study examined initial BBB disruption using Evan's blue (EB), ER stress mechanisms, apoptosis and impulsive-like behavior measured with elevated plus maze (EPM). Large BBB openings were observed immediately following bTBI, and persisted for at least 6 h. Data showed increased mRNA abundance of stress response genes at 3 h, with subsequent increases in the ER stress markers C/EBP homologous protein (CHOP) and growth arrest and DNA damage-inducible protein 34 (GADD34) at 24 h. Caspase-12 and Caspase-3 were both cleaved at 24 h following bTBI. The ER stress inhibitor, salubrinal (SAL), was administered (1 mg/kg i.p.) to investigate its effects on neuronal injury and impulsive-like behavior associated with bTBI. SAL reduced CHOP protein expression, and diminished Caspase-3 cleavage, suggesting apoptosis attenuation. Interestingly, SAL also ameliorated impulsive-like behavior indicative of head trauma. These results suggest SAL plays a role in apoptosis regulation and the pathology of chronic disease. These observations provide evidence that bTBI involves ER stress and that the unfolded protein response (UPR) is a promising molecular target for the attenuation of neuronal injury.
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