ArticleAntioxidants & redox signaling2013
Naturally occurring variation in the Glutathione-S-Transferase 4 gene determines neurodegeneration after traumatic brain injury.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Review
- DA.Frontiers in cell and developmental biology · 2025Article
- Acutely blocking excessive mitochondrial fission prevents chronic neurodegeneration after traumatic brain injury.Cell reports. Medicine · 2024Article
- Article
- Glutathione S-transferases Control astrocyte activation and neuronal health during neuroinflammation.Frontiers in molecular biosciences · 2022Article
- Interaction of oxidative stress and neurotrauma in ALDH2Redox biology · 2020Article
- Glutathione precursors shield the brain from trauma.Neural regeneration research · 2019Article
- GlutathioneScience signaling · 2019Article
- The cysteine-rich whey protein supplement, Immunocal®, preserves brain glutathione and improves cognitive, motor, and histopathological indices of traumatic brain injury in a mouse model of controlled cortical impact.Free radical biology & medicine · 2018Article
- Neuronal Preconditioning Requires the Mitophagic Activity of C-terminus of HSC70-Interacting Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Frontiers of Complex Disease Mechanisms: Membrane Surface Tension May Link Genotype to Phenotype in Glaucoma.Frontiers in cell and developmental biology · 2018Article
- GlutathioneFrontiers in neurology · 2018Article
- Environmental Subconcussive Injury, Axonal Injury, and Chronic Traumatic Encephalopathy.Frontiers in neurology · 2018Review
- Astrocytic Expression of GSTA4 Is Associated to Dopaminergic Neuroprotection in a Rat 6-OHDA Model of Parkinson's Disease.Brain sciences · 2017Article
- Therapies targeting lipid peroxidation in traumatic brain injury.Brain research · 2016Review
- The Genetic Architecture of Murine Glutathione Transferases.PloS one · 2016Article
- A genome-wide association study and biological pathway analysis of epilepsy prognosis in a prospective cohort of newly treated epilepsy.Human molecular genetics · 2014Article
- Perspectives on molecular biomarkers of oxidative stress and antioxidant strategies in traumatic brain injury.BioMed research international · 2014Review
- Cell death and diseases related to oxidative stress: 4-hydroxynonenal (HNE) in the balance.Cell death and differentiation · 2013Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimGenetic factors are important for outcome after traumatic brain injury (TBI), although exact knowledge of relevant genes/pathways is still lacking. We here used an unbiased approach to define differentially activated pathways between the inbred DA and PVG rat strains. The results prompted us to study further if a naturally occurring genetic variation in glutathione-S-transferase alpha 4 (Gsta4) affects the outcome after TBI.
resultsSurvival of neurons after experimental TBI is increased in PVG compared to the DA strain. Global expression profiling analysis shows the glutathione metabolism pathway to be the most regulated between the strains, with increased Gsta4 in PVG among top regulated transcripts. A congenic strain (R5) with a PVG genomic insert containing the Gsta4 gene on DA background displays a reversal of the strain pattern for Gsta4 expression and increased survival of neurons compared to DA. Gsta4 is known to effectively reduce 4-hydroxynonenal (4-HNE), a noxious by-product of lipid peroxidation. Immunostaining of 4-HNE was evident in both rat and human TBI. Intracerebral injection of 4-HNE resulted in neurodegeneration with increased levels of a marker for nerve injury in cerebrospinal fluid of DA compared to R5. INNOVATION: These findings provide strong support for the notion that the inherent capability of coping with increased 4-HNE after TBI affects outcome in terms of nerve cell loss.
conclusionA naturally occurring variation in Gsta4 expression in rats affects neurodegeneration after TBI. Further studies are needed to explore if genetic variability in Gsta4 can be associated to outcome also in human TBI.
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