ArticleJournal of neurochemistry2008
Cytoskeletal protein carbonylation and degradation in experimental autoimmune encephalomyelitis.
Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 68 citations in OpenAlex.
- Complementary PET and MRI of myeloperoxidase activity as a noninvasive surrogate for tissue acrolein in experimental neuroinflammation.NeuroImage · 2026Article
- Neutrophil Heterogeneity in Airway Inflammatory Diseases.Inflammation · 2025Review
- Chemical Carbonylation of Arginine in Peptides and Proteins.Journal of the American Chemical Society · 2025Article
- Oxidative Stress Markers in Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Smouldering Lesion in MS: Microglia, Lymphocytes and Pathobiochemical Mechanisms.International journal of molecular sciences · 2023Review
- Article
- An integrated omics approach to investigate summer mortality of New Zealand Greenshell™ mussels.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- The impact of regional astrocyte interferon-γ signaling during chronic autoimmunity: a novel role for the immunoproteasome.Journal of neuroinflammation · 2020Article
- Reduced expression of the ferroptosis inhibitor glutathione peroxidase-4 in multiple sclerosis and experimental autoimmune encephalomyelitis.Journal of neurochemistry · 2019Article
- The Role of Calpain and Proteasomes in the Degradation of Carbonylated Neuronal Cytoskeletal Proteins in Acute Experimental Autoimmune Encephalomyelitis.Neurochemical research · 2018Article
- proBDNF is modified by advanced glycation end products in Alzheimer's disease and causes neuronal apoptosis by inducing p75 neurotrophin receptor processing.Molecular brain · 2018Article
- Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review.Frontiers in immunology · 2018Review
- Inhibition of cytoskeletal protein carbonylation may protect against oxidative damage in traumatic brain injury.Experimental and therapeutic medicine · 2016Article
- Nrf2-dysregulation correlates with reduced synthesis and low glutathione levels in experimental autoimmune encephalomyelitis.Journal of neurochemistry · 2016Article
- Inhibition of myeloperoxidase at the peak of experimental autoimmune encephalomyelitis restores blood-brain barrier integrity and ameliorates disease severity.Journal of neurochemistry · 2016Article
- The role of Nox-mediated oxidation in the regulation of cytoskeletal dynamics.Current pharmaceutical design · 2015Review
- Targeting pro-resolution pathways to combat chronic inflammation in COPD.Journal of thoracic disease · 2014Review
- Intermittent hypoxia-induced increases in reactive oxygen species activate NFATc3 increasing endothelin-1 vasoconstrictor reactivity.Vascular pharmacology · 2014Article
- Role of alveolar macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2014Review
- Current understanding on the role of standard and immunoproteasomes in inflammatory/immunological pathways of multiple sclerosis.Autoimmune diseases · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Protein carbonylation, the non-enzymatic addition of aldehydes or ketones to specific amino acid residues, has been implicated in the pathophysiology of multiple sclerosis. In this study, we investigated whether protein carbonyls also accumulate in the spinal cord of Lewis rats with acute experimental autoimmune encephalomyelitis (EAE). Western blots analysis after derivatization with dinitrophenyl hydrazine (oxyblot) showed elevated protein carbonylation at the time of maximal clinical disability. During the same period glutathione levels were substantially reduced, suggesting a causal relationship between these two markers. In contrast, lipid peroxidation products accumulated in EAE spinal cord well before the appearance of neurological symptoms. Carbonyl staining was not restricted to inflammatory lesions but present throughout the spinal cord particularly in neuronal cell bodies and axons. By 2-dimensional-oxyblot, we identified several cytoskeletal proteins, including beta-actin, glial acidic fibrillary protein, and the neurofilament proteins as the major targets of carbonylation. These findings were confirmed by pull-down experiments, which also showed an increase in the number of carbonylated beta-actin molecules and a decrease in that of oxidized neurofilament proteins in EAE. These data suggest the possibility that oxidation targets neurofilament proteins for degradation, which may contribute to axonal pathology observed in multiple sclerosis and EAE.
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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.