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The role of SOD‐2 in a mouse model of multiple sclerosis
Author(s) -
Inoue Taeko,
Majid Tabassum,
Quick Ann,
Pautler Robia G.,
Beeton Christine
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.136.11
Subject(s) - pathogenesis , superoxide dismutase , multiple sclerosis , experimental autoimmune encephalomyelitis , immune system , oxidative stress , encephalomyelitis , medicine , demyelinating disease , immunology , experimental pathology , amyotrophic lateral sclerosis , central nervous system , disease , pathology , biology , biochemistry , in vitro
Multiple Sclerosis (MS) is a demyelinating disease of the Central Nervous System (CNS) that can result in debilitation of afflicted individuals. Oxidative stress is suspected of playing a key role in the pathogenesis of this disease; however, the mechanism is poorly understood. We hypothesized that mitochondrial superoxide plays a key role in the pathogenesis of MS and that overexpression of its scavenging enzyme superoxide dismutase‐2 (SOD‐2) would reduce disease severity. We induced experimental autoimmune encephalomyelitis (EAE), a mouse model of MS in SOD‐2 overexpressing (SOD‐2 OV ) and WT control mice and monitored their disease severity for 5 weeks. We found that SOD‐2 OV mice showed a lower disease severity compared to their WT counterparts. At the end of the 5 weeks, mice were imaged using MRI to assess their blood‐brain barrier (BBB) permeability and we found that there was no difference in BBB leakage between genotypes indicating that BBB permeability is not critical in the development and pathogenesis of the disease. Finally, we carried out immunohistochemistry (IHC) and found that there was significantly lower immune infiltrates to be found in the spinal cords of SOD‐2 OV mice compared to WT mice. In conclusion, SOD‐2 overexpression resulted in improved disease severity and lower immune infiltration in a mouse model of MS. Funding sources: RO1: NINDS NS073712 (CB), NIH/NIA R01AG029977 (RGP), NIH/NIDDK P30 DK079638 ‐02 PILOT PJ4 and Mitchell Foundation