ArticleJournal of clinical & cellular immunology2013
Down-regulation of Myelin Gene Expression in Human Oligodendrocytes by Nitric Oxide: Implications for Demyelination in Multiple Sclerosis.
Article in Journal of clinical & cellular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Selective inhibition of TLR2 stimulates the maturation of oligodendroglial progenitor cells to oligodendrocytes.NeuroImmune pharmacology and therapeutics · 2026Article
- Benzoate Drugs for Traumatic Brain Injury.Journal of clinical & experimental immunology · 2026Article
- Build muscles and protect myelin.NeuroImmune pharmacology and therapeutics · 2024Review
- Muscle-building supplement β-hydroxy β-methylbutyrate stimulates the maturation of oligodendroglial progenitor cells to oligodendrocytes.Journal of neurochemistry · 2024Article
- Therapeutic efficacy of cinnamein, a component of balsam of Tolu/Peru, in controlled cortical impact mouse model of TBI.Neurochemistry international · 2024Article
- Evidence for decreased copper associated with demyelination in the corpus callosum of cuprizone-treated mice.Metallomics : integrated biometal science · 2024Article
- Amelioration of experimental autoimmune encephalomyelitis by gemfibrozil in mice via PPARβ/δ: implications for multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Oxidative Stress and the Pathophysiology and Symptom Profile of Schizophrenia Spectrum Disorders.Frontiers in psychiatry · 2021Review
- The BHMT-betaine methylation pathway epigenetically modulates oligodendrocyte maturation.PloS one · 2021Article
- Klotho Is Neuroprotective in the Superoxide Dismutase (SOD1Journal of molecular neuroscience : MN · 2019Article
- Therapeutic Effect of the Mitochondria-Targeted Antioxidant SkQ1 on the Culture Model of Multiple Sclerosis.Oxidative medicine and cellular longevity · 2019Article
- The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2019Article
- Upregulation of Myelin Gene Expression by a Physically-Modified Saline via Phosphatidylinositol 3-Kinase-Mediated Activation of CREB: Implications for Multiple Sclerosis.Neurochemical research · 2018Article
- Article
- Oxidative stress, prefrontal cortex hypomyelination and cognitive symptoms in schizophrenia.Translational psychiatry · 2017Review
- Oligodendrocyte Nf1 Controls Aberrant Notch Activation and Regulates Myelin Structure and Behavior.Cell reports · 2017Article
- Role of Gasotransmitters in Oxidative Stresses, Neuroinflammation, and Neuronal Repair.BioMed research international · 2017Review
- Hydroxycitric acid ameliorates inflammation and oxidative stress in mouse models of multiple sclerosis.Neural regeneration research · 2016Article
- The crucial role of Erk2 in demyelinating inflammation in the central nervous system.Journal of neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a chronic autoimmune demyelinating disorder of the central nervous system (CNS) with unknown etiology. Several studies have shown that demyelination in MS is caused by proinflammatory mediators and nitric oxide (NO), which is released by perivascular infiltrates and/or activated glial cells. Both endogenous NO released by microglia and astrocytes; and NO generated from exogenous NO donors are known to induce oligodendrocytes death. However, the molecular mechanism of oligodendroglial death is poorly understood. Here we explore the role of NO in modulating the expression of myelin-specific genes that leads to oligodendroglial death. We investigated the effect of NO on the expression of myelin basic protein (MBP), 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), myelin oligodendrocyte glycoprotein (MOG), and proteolipid protein (PLP) in human primary oligodendrocytes. Combination of IFN-γ and bacterial lipopolysaccharide (LPS) or double stranded RNA in the form of polyIC induced the production of NO and decreased the expression of myelin gene in human fetal mixed glial cultures. Either a scavenger of NO (PTIO) or an inhibitor of inducible nitric oxide synthase (L-NIL) abrogated (LPS+IFN-γ)- and polyIC-mediated suppression of myelin genes in human mixed glial cells. The role of NO was further corroborated by the inhibition of myelin gene expression in purified human oligodendroglia by several NO donors including SNP, NOC-7, SIN-1, and SNAP. This study illustrates a novel biological role of NO in down-regulating the expression of myelin genes preceding the death of oligodendrocytes.
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Registered trials
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