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- W2016204866 abstract "Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). It is the most common neurological disorder in young adults. MS presents with different disease courses, all of them affecting white matter and grey matter of the CNS. For basic MS research, the animal model experimental autoimmune encephalomyelitis (EAE) is widely used. It can be elicited in many different species either actively by injection of CNS antigens or passively by injection of CNS antigen-specific autoreactive T cells. Our study is based on formalin-fixed paraffin-embedded human autopsy material and freshly frozen experimental animal tissue. After detailed neuropathological characterization, we microdissected selected white matter and grey matter (cortical) lesions from acute as well as secondary progressive MS cases. In parallel, passive EAE was elicited by injection of MBP-specific CD4+ T cells in wild-type Lewis rats and the affected lumbar spinal cord was collected at the peak of the disease. We isolated mRNA from the microdissected MS lesions or freshly frozen EAE spinal cords and did whole-genome microarray approaches or customized TaqMan® qPCR arrays. Focusing on genes involved in oxidative tissue injury, the expression data showed substantial differences between MS and its animal model EAE. While mitochondrially-encoded genes were strongly dysregulated in white matter MS lesions as well as in cortical MS lesions, their transcription level was largely unchanged in the EAE-afflicted spinal cords. Regarding enzymes involved in radical production, we could attribute the components of the NADPH oxidase (NOS) 2 complex and nitric oxide synthase 2 (Nos2, iNos) to inflammatory infiltrates in EAE. In MS, however, a more widespread expression pattern of genes related to oxidative injury was observed. Via immunohistochemistry we confirmed the differences in gene expression patterns and revealed major differences in microglia activation, in the presence of oxidized DNA and lipids, in mitochondrial injury and in iron metabolism between MS and different EAE models. Thus, currently available rodent models only poorly reflect the mechanisms of oxidative tissue injury seen in patients with progressive MS." @default.
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- W2016204866 date "2014-10-01" @default.
- W2016204866 modified "2023-09-26" @default.
- W2016204866 title "Molecular mechanisms of oxidative tissue injury differ between multiple sclerosis and experimental disease models" @default.
- W2016204866 doi "https://doi.org/10.1016/j.jneuroim.2014.08.294" @default.
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