ArticleMolecular genetics and metabolism2018
Arginase overexpression in neurons and its effect on traumatic brain injury.
Article in Molecular genetics and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- ARG1-polyamine axis: cell-type-specific functions in disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2026Review
- Gut to brain: essential micronutrient and trace element manganese transport, function and toxicity.Frontiers in physiology · 2025Review
- Non-Receptor Tyrosine Kinases: Their Structure and Mechanistic Role in Tumor Progression and Resistance.Cancers · 2024Review
- Assessment of cerebrovascular alterations induced by inflammatory response and oxidative-nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy.Scientific reports · 2024Article
- Possible Role of Cellular Polyamine Metabolism in Neuronal Apoptosis.Current medical science · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- Potential preventive markers in the intracerebral hemorrhage process are revealed by serum untargeted metabolomics in mice using hypertensive cerebral microbleeds.Frontiers in endocrinology · 2023Article
- The role of L-arginine metabolism in neurocritical care patients.Neural regeneration research · 2022Review
- Preclinical investigation of Pegylated arginase 1 as a treatment for retina and brain injury.Experimental neurology · 2022Article
- IGF1 Gene Therapy Reversed Cognitive Deficits and Restored Hippocampal Alterations After Chronic Spinal Cord Injury.Molecular neurobiology · 2021Article
- Intrathecal and systemic alterations of L-arginine metabolism in patients after intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update.International journal of molecular sciences · 2021Review
- Review
- Changes in inflammatory gene expression in brain tissue adjacent and distant to a viable cyst in a rat model for neurocysticercosis.PLoS neglected tropical diseases · 2021Article
- IL-22 hinders antiviral T cell responses and exacerbates ZIKV encephalitis in immunocompetent neonatal mice.Journal of neuroinflammation · 2020Article
- Metabolomics Deciphers Potential Targets of Xuefu Zhuyu Decoction Against Traumatic Brain Injury in Rat.Frontiers in pharmacology · 2020Article
- Arginase Pathway in Acute Retina and Brain Injury: Therapeutic Opportunities and Unexplored Avenues.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Arginine is a semi-essential amino acid which serves as a substrate for nitric oxide (NO) production by nitric oxide synthase (NOS) and a precursor for various metabolites including ornithine, creatine, polyamines, and agmatine. Arginase competes with nitric oxide synthase for substrate arginine to produce orthinine and urea. There is contradictory evidence in the literature on the role of nitric oxide in the pathophysiology of traumatic brain injury (TBI). These contradictory perspectives are likely due to different NOS isoforms - endothelial (eNOS), inducible (iNOS) and neuronal (nNOS) which are expressed in the central nervous system. Of these, the role of nNOS in acute injury remains less clear. This study aimed to employ a genetic approach by overexpressing arginase isoforms specifically in neurons using a Thy-1 promoter to manipulate cell autonomous NO production in the context of TBI. The hypothesis was that increased arginase would divert arginine from pathological NO production. We generated 2 mouse lines that overexpress arginase I (a cytoplasmic enzyme) or arginase II (a mitochondrial enzyme) in neurons of FVB mice. We found that two-weeks after induction of controlled cortical injury, overexpressing arginase I but not arginase II in neurons significantly reduced contusion size and contusion index compared to wild-type (WT) mice. This study establishes enhanced neuronal arginase levels as a strategy to affect the course of TBI and provides support for the potential role of neuronal NO production in this condition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.