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Abstract Title:

Forced running exercise mitigates radiation-induced cognitive deficits via regulated DNA hydroxymethylation.

Abstract Source:

Epigenomics. 2020 Feb 11. Epub 2020 Feb 11. PMID: 32041423

Abstract Author(s):

Junjun Zhang, Junyan Li, Yiwen Zhu, Zhigang Miao, Ye Tian

Article Affiliation:

Junjun Zhang

Abstract:

Roles of forced running exercise (FE) in remediation of neurogenesis inhibition and radiation-induced cognitive dysfunction were investigated in a whole-brain irradiation mice model via the regulation of DNA 5-hydroxymethylation modification (5 hmC) and its catalytic enzymes ten-eleven translocation (Tet) proteins.Hippocampal neurogenesis and cognitive function, DNA 5 hmC level and Tet expression were determined in mice.The expression of DNA 5 hmC and Tet2, brain-derived neurotrophic factor significantly decreased in hippocampus postradiation. FE mitigated radiation-induced neurogenesis deficits and cognitive dysfunction. Furthermore, FE increased 5 hmC and brain-derived neurotrophic factor expression. SC1, a Tet inhibitor, reversed partly such changes.Tet-mediated 5 hmC modification represents a kind of diagnostic biomarkers of radiation-induced cognitive dysfunction. Targeting Tet-related epigenetic modification may be a novel therapeutic strategy for radiation-induced brain injury.

Study Type : Animal Study

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Sayer Ji
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