ArticleInternational journal of critical illness and injury science2012
Mitochondrial targeted neuron focused genes in hippocampus of rats with traumatic brain injury.
Article in International journal of critical illness and injury science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Mesenchymal Stem Cells in the Treatment of Traumatic Brain Injury.Frontiers in neurology · 2017Review
- Near-infrared photonic energy penetration: can infrared phototherapy effectively reach the human brain?Neuropsychiatric disease and treatment · 2015Review
- Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery.Frontiers in neurology · 2015Review
- Identification of serum microRNA signatures for diagnosis of mild traumatic brain injury in a closed head injury model.PloS one · 2014Article
- Impact of repeated stress on traumatic brain injury-induced mitochondrial electron transport chain expression and behavioral responses in rats.Frontiers in neurology · 2013Article
- Identification of Serum Biomarkers for Blast-induced Traumatic Brain Injuries: LowIn vivo (Athens, Greece)Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextMild traumatic brain injury (mTBI) represents a major health problem in civilian populations as well as among the military service members due to (1) lack of effective treatments, and (2) our incomplete understanding about the progression of secondary cell injury cascades resulting in neuronal cell death due to deficient cellular energy metabolism and damaged mitochondria.
aimsThe aim of this study was to identify and delineate the mitochondrial targeted genes responsible for altered brain energy metabolism in the injured brain. SETTINGS AND
designRats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed up for 7 days. MATERIALS AND
methodsRats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed for 7 days. The severity of brain injury was evaluated by the neurological severity scale-revised (NSS-R) at 3 and 5 days post TBI and immunohistochemical analyses at 7 days post TBI. The expression profiles of mitochondrial-targeted genes across the hippocampus from TBI and naïe rats were also examined by oligo-DNA microarrays.
resultsNSS-R scores of TBI rats (5.4 ± 0.5) in comparison to naïe rats (3.9 ± 0.5) and H and E staining of brain sections suggested a mild brain injury. Bioinformatics and systems biology analyses showed 31 dysregulated genes, 10 affected canonical molecular pathways including a number of genes involved in mitochondrial enzymes for oxidative phosphorylation, mitogen-activated protein Kinase (MAP), peroxisome proliferator-activated protein (PPAP), apoptosis signaling, and genes responsible for long-term potentiation of Alzheimer's and Parkinson's diseases.
conclusionsOur results suggest that dysregulated mitochondrial-focused genes in injured brains may have a clinical utility for the development of future therapeutic strategies aimed at the treatment of TBI.
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