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The alteration of 5-hydroxymethylcytosine modification contributes to ischemic brain injury [5hmC-seq]


ABSTRACT: Epigenetic modifications, such as cytosine methylation and histone modification, have been shown involved in the pathology of ischemic brain injury. Recent works have implicated 5-hydroxymethylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC) through the oxidation by Ten-Eleven Translocation (TET) enzymes, in DNA methylation-related plasticity. In this study we show that 5hmC abundance could be induced to increase by ischemia injury. Genome-wide profiling of 5hmC identified differentially hydroxymethylated regions (DhMRs) associated with ischemic injury and DhMRs were found enriched among the genes involved in cell junction, neuronal morphogenesis and neurodevelopment. These data together suggest that 5hmC modification could serve as a potential therapeutic target for the treatment of ischemic stroke. To determine the genome-wide 5hmC distribution in both ischemic injury (I/R) and control mice (C57BL/6), we employed a previously established chemical labeling and affinity purification method, coupled with high-throughput sequencing (Song et al, Nature Biotechnology, 2011). The ischemic or matched control brain tissues from three pairs of ischemic mice and control mice were used for the analyses.

ORGANISM(S): Mus musculus

SUBMITTER: Peng Jin 

PROVIDER: E-GEOD-67188 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Altering 5-hydroxymethylcytosine modification impacts ischemic brain injury.

Miao Zhigang Z   He Yuquan Y   Xin Ning N   Sun Miao M   Chen Li L   Lin Li L   Li Jizhen J   Kong Jiming J   Jin Peng P   Xu Xingshun X  

Human molecular genetics 20150730 20


Epigenetic modifications such as cytosine methylation and histone modification are linked to the pathology of ischemic brain injury. Recent research has implicated 5-hydroxymethylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC) via oxidation by ten-eleven translocation (Tet) enzymes, in DNA methylation-related plasticity. Here we show that 5hmC abundance was increased after ischemic injury, and Tet2 was responsible for this increase; furthermore, inhibiting Tet2 expression abolish  ...[more]

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