Effects of Transient Cerebral Ischemia on the Expression of DNA Methyltransferase 1 in the Gerbil Hippocampal CA1 Region |
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Authors: | Jae-Chul Lee Joon Ha Park Bing Chun Yan In Hye Kim Geum-Sil Cho Dooil Jeoung Young-Geun Kwon Young-Myeong Kim Yun Lyul Lee Hyung-Cheul Shin Moo-Ho Won |
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Institution: | 1. Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea 2. Department of Neuroscience, College of Medicine, Korea University, Seoul, 136-705, South Korea 3. Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, 200-701, South Korea 4. Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea 5. Vascular System Research Center, Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea 6. Department of Physiology, College of Medicine, Institute of Neurodegeneration and Neuroregeneration, Hallym University, Chuncheon, 200-701, South Korea
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Abstract: | DNA methylation is a key epigenetic modification of DNA that is catalyzed by DNA methyltransferases (Dnmt). Increasing evidences suggest that DNA methylation in neurons regulates synaptic plasticity as well as neuronal network activity. In the present study, we investigated the changes in DNA methyltransferases 1 (Dnmt1) immunoreactivity and its protein levels in the gerbil hippocampal CA1 region after 5 min of transient global cerebral ischemia. CA1 pyramidal neurons were well stained with NeuN (a neuron-specific soluble nuclear antigen) antibody in the sham-group, Four days after ischemia–reperfusion (I–R), NeuN-positive (+) cells were significantly decreased in the stratum pyramidale (SP) of the CA1 region, and many Fluro-Jade B (a marker for neuronal degeneration)+ cells were observed in the SP. Dnmt1 immunoreactivity was well detected in all the layers of the sham-group. Dnmt1 immunoreactivity was hardly detected only in the stratum pyramidale of the CA1 region from 4 days post-ischemia; however, at these times, Dnmt1 immunoreactivity was newly expressed in GABAergic interneurons or astrocytes in the ischemic CA1 region. In addition, the level of Dnmt1 was lowest at 4 days post-ischemia. In brief, both the Dnmt1 immunoreactivity and protein levels were distinctively decreased in the ischemic CA1 region 4 days after transient cerebral ischemia. These results indicate that the decrease of Dnmt1 expression at 4 days post-ischemia may be related to ischemia-induced delayed neuronal death. |
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