Journal
EPIGENOMICS
Volume 11, Issue 3, Pages 323-335Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/epi-2018-0162
Keywords
5-hydroxymethylcytosine; BDNF; experimental autoimmune encephalomyelitis; multiple sclerosis; spinal cord; Ten-eleven translocation enzymes
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Funding
- National Key R&D Program of China [2017YFE0103700]
- National Natural Science Foundation of China [81601154]
- Natural Science Foundation of Jiangsu Province [BK20141281]
- Special Foundation Project on the Prospective Study of Social Development in Jiangsu Province [BE2013911]
- Jiangsu Six Categories of Talent Summit Fund [WSW-133]
- Social Development of Science and Technology Research Project in Yangzhou [YZ2011082]
- Jiangsu Province 333 talent Project [BRA2016159]
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Aim: Roles of DNA 5-hydroxymethylcytosine (5hmC) in myelin repair were investigated in an experimental autoimmune encephalomyelitis (EAE) mouse model via its regulation on BDNF. Methods: DNA 5hmC level and its limiting enzymes were detected in EAE mice. Results: Global 5hmC modification, Tet1 and Tet2 significantly decreased in the spinal cord tissues of EAE mice. BDNF protein and mRNA decreased and were highly associated with BDNF 5hmC. Vitamin C, a Tet co-factor, increased global DNA 5hmC and reduced the neurological deficits at least by increasing BDNF5hmC modification and protein levels. Conclusion: Tet protein-mediated 5hmC modifications represent a critical target involved in EAE-induced myelin damage. Targeting epigenetic modification may be a therapeutic strategy for multiple sclerosis.
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