Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune Encephalomyelitis
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| Titel: | Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune Encephalomyelitis |
|---|---|
| Autoren: | Dunham, Jordon, Bauer, Jan, Campbell, Graham R., Mahad, Don J., van Driel, Nikki, van der Pol, Susanne M.A., 't Hart, Bert A., Lassmann, Hans, Laman, Jon D., van Horssen, Jack, Kap, Yolanda S. |
| Quelle: | Dunham, J, Bauer, J, Campbell, G R, Mahad, D J, van Driel, N, van der Pol, S M A, 't Hart, B A, Lassmann, H, Laman, J D, van Horssen, J & Kap, Y S 2017, 'Oxidative injury and iron redistribution are pathological hallmarks of marmoset experimental autoimmune encephalomyelitis', Journal of Neuropathology and Experimental Neurology, vol. 76, no. 6, pp. 467-478. https://doi.org/10.1093/jnen/nlx034 |
| Verlagsinformationen: | Oxford University Press (OUP), 2017. |
| Publikationsjahr: | 2017 |
| Schlagwörter: | EXPRESSION, Male, 0301 basic medicine, Encephalomyelitis, Autoimmune, Experimental, Experimental autoimmune encephalomyelitis (EAE), Iron, INCOMPLETE FREUNDS-ADJUVANT, Nitric Oxide Synthase Type II, 7. Clean energy, Nonheme Iron Proteins, Multiple sclerosis, 03 medical and health sciences, MYELIN OLIGODENDROCYTE GLYCOPROTEIN, NADPH OXIDASE, Animals, HSP70 Heat-Shock Proteins, Tissue Distribution, Neurodegeneration, NITRIC-OXIDE SYNTHASE, Myelin Sheath, DAMAGE, 0303 health sciences, Superoxide Dismutase, NEURODEGENERATION, MULTIPLE-SCLEROSIS LESIONS, NADPH Oxidases, CALLITHRIX-JACCHUS, COMMON MARMOSETS, Callithrix, Immunohistochemistry, Marmoset, Oxidative Stress, 13. Climate action, Female, Reactive oxygen species, Demyelinating Diseases |
| Beschreibung: | Oxidative damage and iron redistribution are associated with the pathogenesis and progression of multiple sclerosis (MS), but these aspects are not entirely replicated in rodent experimental autoimmune encephalomyelitis (EAE) models. Here, we report that oxidative burst and injury as well as redistribution of iron are hallmarks of the MS-like pathology in the EAE model in the common marmoset. Active lesions in the marmoset EAE brain display increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (p22phox, p47phox, and gp91phox) and inducible nitric oxide synthase immunoreactivity within lesions with active inflammation and demyelination, coinciding with enhanced expression of mitochondrial heat-shock protein 70 and superoxide dismutase 1 and 2. The EAE lesion-associated liberation of iron (due to loss of iron-containing myelin) was associated with altered expression of the iron metabolic markers FtH1, lactoferrin, hephaestin, and ceruloplasmin. The enhanced expression of oxidative damage markers in inflammatory lesions indicates that the enhanced antioxidant enzyme expression could not counteract reactive oxygen and nitrogen species-induced cellular damage, as is also observed in MS brains. This study demonstrates that oxidative injury and aberrant iron distribution are prominent pathological hallmarks of marmoset EAE thus making this model suitable for therapeutic intervention studies aimed at reducing oxidative stress and associated iron dysmetabolism. |
| Publikationsart: | Article |
| Sprache: | English |
| ISSN: | 1554-6578 0022-3069 |
| DOI: | 10.1093/jnen/nlx034 |
| Zugangs-URL: | https://academic.oup.com/jnen/article-pdf/76/6/467/17231416/nlx034.pdf https://pubmed.ncbi.nlm.nih.gov/28505283 https://research.rug.nl/en/publications/1e3e06c4-3f6d-457c-a339-c3b96b687dae https://hdl.handle.net/11370/1e3e06c4-3f6d-457c-a339-c3b96b687dae https://doi.org/10.1093/jnen/nlx034 https://www.rug.nl/research/portal/en/publications/oxidative-injury-and-iron-redistribution-are-pathological-hallmarks-of-marmoset-experimental-autoimmune-encephalomyelitis(1e3e06c4-3f6d-457c-a339-c3b96b687dae).html https://core.ac.uk/display/92642973 https://academic.oup.com/jnen/article/76/6/467/3826544 https://research.vumc.nl/en/publications/oxidative-injury-and-iron-redistribution-are-pathological-hallmar https://europepmc.org/abstract/MED/28505283 https://www.ncbi.nlm.nih.gov/pubmed/28505283 https://research.vumc.nl/en/publications/b014dcb4-a483-4374-8372-7011c1e7a602 https://pure.amsterdamumc.nl/en/publications/cf7673e9-6caf-4977-82de-01f923cc8348 https://doi.org/10.1093/jnen/nlx034 |
| Rights: | taverne |
| Dokumentencode: | edsair.doi.dedup.....53f5d25d87e50e4fe22830ec7e7ced33 |
| Datenbank: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstract: | Oxidative damage and iron redistribution are associated with the pathogenesis and progression of multiple sclerosis (MS), but these aspects are not entirely replicated in rodent experimental autoimmune encephalomyelitis (EAE) models. Here, we report that oxidative burst and injury as well as redistribution of iron are hallmarks of the MS-like pathology in the EAE model in the common marmoset. Active lesions in the marmoset EAE brain display increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (p22phox, p47phox, and gp91phox) and inducible nitric oxide synthase immunoreactivity within lesions with active inflammation and demyelination, coinciding with enhanced expression of mitochondrial heat-shock protein 70 and superoxide dismutase 1 and 2. The EAE lesion-associated liberation of iron (due to loss of iron-containing myelin) was associated with altered expression of the iron metabolic markers FtH1, lactoferrin, hephaestin, and ceruloplasmin. The enhanced expression of oxidative damage markers in inflammatory lesions indicates that the enhanced antioxidant enzyme expression could not counteract reactive oxygen and nitrogen species-induced cellular damage, as is also observed in MS brains. This study demonstrates that oxidative injury and aberrant iron distribution are prominent pathological hallmarks of marmoset EAE thus making this model suitable for therapeutic intervention studies aimed at reducing oxidative stress and associated iron dysmetabolism. |
|---|---|
| ISSN: | 15546578 00223069 |
| DOI: | 10.1093/jnen/nlx034 |