LPS mediated injury to oligodendrocytes is mediated by the activation of nNOS: Relevance to human demyelinating disease

Yao, Song‐Yi; Pandey, Pragati; Ljunggren-Rose, Asa; Subramaniam, Sriram

doi:10.1016/j.niox.2009.12.001

Cited by 20 publications

(14 citation statements)

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“…nNOS and eNOS are constitutively expressed and require calcium and calmodulin for activation, whereas iNOS is largely calcium independent and induced in inflammatory conditions (Knowles and Moncada, 1994). Although nNOS and eNOS have been shown to be elevated in experimental autoimmune encephalomyelitis (EAE), one of the commonly used animal models of MS (Wu and Tsirka, 2009;Yao et al, 2010), iNOS induction in reactive microglia/macrophages and astrocytes is believed to be the predominant source of NO (Broholm et al, 2004;Sun et al, 2010). It is known that NO is neither a potent oxidant nor a strong reductant (Calabrese et al, 2009), but it can rapidly react with superoxide to produce the powerful oxidant peroxynitrite (Beckman et al, 1990;Pacher et al, 2007).…”

mentioning

confidence: 99%

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Vana

Ribeiro

et al. 2011

Neuroscience

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mentioning

confidence: 99%

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Vana

Ribeiro

et al. 2011

Neuroscience

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“…Nitric oxide plays a major role in a number of aspects of MS through triggering inflammatory factors, inducing neuronal death, and causing demyelination (Brenner et al 2001;Encinas et al 2005;Yao et al 2010). Increased serum and CSF concentrations of NO metabolites have been noted in MS patients, and have been suggested to cause damage to myelin and oligodendrocytes via lipid peroxidation (Speciale et al 2000;Kouhsar et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Effects of an aqueous extract of North American ginseng on MOG_(35–55)-induced EAE in mice

Bowie

Roscoe

Lui

et al. 2012

Can. J. Physiol. Pharmacol.

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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system, in which the release of reactive oxygen species by infiltrating immune cells contributes to demyelination. American ginseng ( Panax quinquefolius ) is a natural health product with numerous beneficial properties, including anti-inflammatory and anti-oxidant effects. The purpose of this study was to determine whether ginseng could influence the course of the disease experimental autoimmune encephalomyelitis (EAE), an animal model of MS. C57BL/6J mice were immunized with MOG((35-55)) peptide to induce EAE. After clinical disease appeared, mice received either oral doses of an aqueous extract of ginseng (150 mg/kg body mass), or the vehicle. Clinical symptoms were recorded, and spinal cord tissue samples were analyzed for pathological signs of disease. The aqueous extract of ginseng significantly decreased (i) clinical signs of EAE, (ii) levels of circulating TNF-α, and (iii) central nervous system immunoreactive iNOS and demyelination scores, without a change in other neuropathological measures. This study shows that an aqueous extract of ginseng may be able to attenuate certain signs of EAE, suggesting that it may be a useful adjuvant therapy for MS.

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“…TLRs receptors, expressed mainly in sentinel cells of the immune system (50), also have important functions in oligodendrocytes (3,49). Yao et al through the in vitro and in vivo investigations on TLR mediated injury of demyelination by lipopolysaccharide, showed the involvement of increased NO production, and more importantly, a susceptibility of the oligodendrocytes to NO-mediated cell death by the activation of nNOS but not of iNOS (59,60).…”

Section: +mentioning

confidence: 99%

“…Different isoforms of nitric oxide synthase (NOS) produce NO. For instance, neuronal NOS (nNOS) is present exclusively in neurons and the inducible NOS (iNOS) can be activated in glial cells; iNOS and nNOS are present in oligodendrocytes (59,60). Other than the physiological actions, NO can cause cellular damage and act as a key mediator of neurodegeneration in many diseases, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and stroke (20).…”

mentioning

confidence: 99%

“…Other than the physiological actions, NO can cause cellular damage and act as a key mediator of neurodegeneration in many diseases, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and stroke (20). Moreover, there is the evidence for association of nNOS activation with the loss of oligodendrocytes and demyelination (59,60).…”

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confidence: 99%

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Noscapine protects OLN-93 oligodendrocytes from ischemia-reperfusion damage: Calcium and nitric oxide involvement

Nadjafi

Rahbar‐Roshandel

2015

Acta Physiologica Hungarica

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This study was carried out to evaluate the effects of noscapine, a benzylisoquinoline alkaloid from opium poppy, on oligodendrocyte during ischemia/reperfusion-induced excitotoxic injury. Changes in intracellular calcium levels due to chemical ischemia and nitric oxide (NO) production during ischemia/reperfusion were evaluated as the hallmarks of ischemia-derived excitotoxic event. OLN-93 cell line (a permanent immature rat oligodendrocyte) was used as a model of oligodendrocyte. 30-or 60-minute-oxygen-glucose deprivation/24 hours reperfusion were used to induce excitotoxicity. MTT (3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide) assay was used to evaluate cell viability. Ratiometric fluorescence microscopy using Ca 2+-sensitive indicator Fura-2/AM was utilized to assess intracellular calcium levels. NO production was evaluated by Griess method. Noscapine (4 μM) significantly attenuated intracellular Ca 2+ elevation (P < 0.001). Also, noscapine significantly decreased NO production during a 30-minute oxygen-glucose deprivation/reperfusion (P < 0.01). The inhibitory effect of noscapine (4 μM) on intracellular Ca 2+ was greater than ionotropic glutamate receptors antagonists. Noscapine is protective against ischemia/reperfusion-induced excitotoxic injury in OLN-93 oligodendrocyte. This protective effect seems to be related to attenuation of intracellular Ca 2+ overload and NO production.

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LPS mediated injury to oligodendrocytes is mediated by the activation of nNOS: Relevance to human demyelinating disease

Cited by 20 publications

References 54 publications

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Effects of an aqueous extract of North American ginseng on MOG_(35–55)-induced EAE in mice

Noscapine protects OLN-93 oligodendrocytes from ischemia-reperfusion damage: Calcium and nitric oxide involvement

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LPS mediated injury to oligodendrocytes is mediated by the activation of nNOS: Relevance to human demyelinating disease

Cited by 20 publications

References 54 publications

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

Effects of an aqueous extract of North American ginseng on MOG(35–55)-induced EAE in mice

Noscapine protects OLN-93 oligodendrocytes from ischemia-reperfusion damage: Calcium and nitric oxide involvement

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Effects of an aqueous extract of North American ginseng on MOG_(35–55)-induced EAE in mice