AI Article Synopsis
- Changes in the xCT subunit of the cystine/glutamate antiporter system xc(-) are linked to several neurological disorders, including multiple sclerosis (MS), leading to interest in targeting it for new treatments.
- This study utilized Theiler's murine encephalomyelitis virus (TMEV) infection in both cell cultures and animal models to investigate the role of system xc(-) in MS.
- Findings indicated that TMEV infection did not alter xCT protein levels or the activity of system xc(-) in macrophages or mouse brains, suggesting that TMEV is not a suitable model for studying system xc(-) in the context of MS.
Article Abstract
Changes in the expression of xCT, the specific subunit of system xc(-) or the cystine/glutamate antiporter, have been associated with several neurological disorders and system xc(-) was recently proposed as a potential target for the development of new treatment strategies for multiple sclerosis (MS). In this study we used Theiler's murine encephalomyelitis virus (TMEV) infection, both in vitro and in vivo, as a model to further evaluate the involvement of system xc(-) in MS. Protein levels of xCT, as well as activity of system xc(-) were unaffected in RAW264.7 macrophages after infection with the demyelinating DA strain of TMEV. Also, protein expression of xCT remained stable in spinal cord and brain of FVB mice 1-2 and 6 weeks after intracranial injection of the DA strain of TMEV. These results demonstrate that TMEV infection of macrophages or FVB mice has no effect on system xc(-) and as such cannot be used as a model to study the involvement of system xc(-) in MS.
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| http://dx.doi.org/10.1016/j.neulet.2015.03.026 | DOI Listing |
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