ArticleBrain research2016
Targeting the nNOS/peroxynitrite/calpain system to confer neuroprotection and aid functional recovery in a mouse model of TBI.
Article in Brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Calpain Inhibitors as Potential Therapeutic Modulators in Neurodegenerative Diseases.Neurochemical research · 2022Pooled it
- The time-dependent changes in a mouse model of traumatic brain injury with motor dysfunction.PloS one · 2024Article
- Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.Nitric oxide : biology and chemistry · 2022Review
- Synaptamide Modulates Astroglial Activity in Mild Traumatic Brain Injury.Marine drugs · 2022Article
- Vascular and immunopathological role of Asymmetric Dimethylarginine (ADMA) in Experimental Autoimmune Encephalomyelitis.Immunology · 2021Article
- MicroRNA-137-3p Protects PC12 Cells Against Oxidative Stress by Downregulation of Calpain-2 and nNOS.Cellular and molecular neurobiology · 2021Article
- Role of the Polyol Pathway in Locomotor Recovery and Wallerian Degeneration after Spinal Cord Contusion Injury.Neurotrauma reports · 2021Article
- Role of Nitric Oxide in Neurodegeneration: Function, Regulation, and Inhibition.Current neuropharmacology · 2021Review
- Targeting GSNOR for functional recovery in a middle-aged mouse model of stroke.Brain research · 2020Article
- Asymmetric dimethylarginine exacerbates cognitive dysfunction associated with cerebrovascular pathology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Antioxidant Therapies in Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2020Review
- Ormosanine improves neuronal functions in spinal cord-injured rats by blocking peroxynitrite/calpain activity.Translational neuroscience · 2020Article
- Therapeutic exploitation of the S-nitrosoglutathione/S-nitrosylation mechanism for the treatment of contusion spinal cord injury.Neural regeneration research · 2019Article
- Regulation of endothelial barrier integrity by redox-dependent nitric oxide signaling: Implication in traumatic and inflammatory brain injuries.Nitric oxide : biology and chemistry · 2019Article
- Combined treatment with GSNO and CAPE accelerates functional recovery via additive antioxidant activities in a mouse model of TBI.Journal of neuroscience research · 2018Article
- Isoliquiritigenin Provides Protection and Attenuates Oxidative Stress-Induced Injuries via the Nrf2-ARE Signaling Pathway After Traumatic Brain Injury.Neurochemical research · 2018Article
- Arginase overexpression in neurons and its effect on traumatic brain injury.Molecular genetics and metabolism · 2018Article
- Amelioration of spinal cord injury in rats by blocking peroxynitrite/calpain activity.BMC neuroscience · 2018Article
- GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α.Behavioural brain research · 2018Article
- The effects of 7-nitroindazole on serum neuron-specific enolase and astroglia-derived protein (S100β) levels after traumatic brain injury.Experimental and therapeutic medicine · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) derails nitric oxide (NO)-based anti-inflammatory and anti-excitotoxicity mechanisms. NO is consumed by superoxide to form peroxynitrite, leading to decreased NO bioavailability for S-nitrosoglutathione (GSNO) synthesis and regulation of neuroprotective pathways. Neuronal peroxynitrite is implicated in neuronal loss and functional deficits following TBI. Using a contusion mouse model of TBI, we investigated mechanisms for the opposed roles of GSNO versus peroxynitrite for neuroprotection and functional recovery. TBI was induced by controlled cortical impact (CCI) in adult male mice. GSNO treatment at 2h after CCI decreased the expression levels of phospho neuronal nitric oxide synthase (pnNOS), alpha II spectrin degraded products, and 3-NT, while also decreasing the activities of nNOS and calpains. Treatment of TBI with FeTPPS, a peroxynitrite scavenger, had effects similar to GSNO treatment. GSNO treatment of TBI also reduced neuronal degeneration and improved neurobehavioral function in a two-week TBI study. In a cell free system, SIN-1 (a peroxynitrite donor and 3-nitrotyrosinating agent) increased whereas GSNO (an S-nitrosylating agent) decreased calpain activity, and these activities were reversed by, respectively, FeTPPS and mercuric chloride, a cysteine-NO bond cleaving agent. These data indicate that peroxynitrite-mediated activation and GSNO-mediated inhibition of the deleterious nNOS/calpain system play critical roles in the pathobiology of neuronal protection and functional recovery in TBI disease. Given GSNO׳s safety record in other diseases, its neuroprotective efficacy and promotion of functional recovery in this TBI study make low-dose GSNO a potential candidate for preclinical evaluation.
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Registered trials
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