Effects of cerebral ischemia in mice lacking DNA methyltransferase I in post-mitotic neurons
Effects of cerebral ischemia in mice lacking DNA methyltransferase I in post-mitotic neurons
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DOI：
10.1097/00001756-200112040-00032
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发表时间：
2001-12-04
期刊：
影响因子：
1.7
通讯作者：
Jaenisch, R
中科院分区：
文献类型：
--
作者：
Endres, M;Fan, GP;Jaenisch, R
DNA甲基化对于控制基因表达是重要的，并且由DNA甲基转移酶（Dnmt I）催化，所述DNA甲基转移酶（Dnmt I）是脑中丰富的酶。我们最近证明，表达降低水平的DnmtI的小鼠免受脑缺血。在这里，我们使用的cre/IoxP系统产生条件突变体，缺乏Dnmt我在有丝分裂后的神经元的出生后的大脑。我们证明了条件等位基因（DnmtI（llox/+））杂合子动物在Ih大脑中动脉闭塞/再灌注后的梗死显著小于其野生型窝仔。令人惊讶的是，在有丝分裂后神经元中缺失DnmtI的小鼠（DnmtI（Ilox/c））没有受到保护。总之，我们证明，有丝分裂后神经元中DnmtI水平的降低，但不是其缺失，可以保护缺血性脑损伤。NeuroReport 12：3763-3766（C）2001 Lippincott威廉姆斯和威尔金斯。
DNA methylation is important for controlling gene expression and is catalyzed by DNA methyltransferase (DnmtI) an enzyme abundant in brain. We recently demonstrated that, mice expressing reduced levels of DnmtI are protected from cerebral ischemia. Here, we used the cre/IoxP system to produce conditional mutants that lack Dnmt I in postmitotic neurons of the postnatal brain. We demonstrate that animals heterozygous for the conditional allele (DnmtI(llox/+)) have significantly smaller infarcts following Ih middle cerebral artery occlusion/reperfusion compared to their wildtype litters. Surprisingly, mice with a deletion of DnmtI in post-mitotic neurons (DnmtI(llox/c)) were not protected. In conclusion, we demonstrate that reduced levels of DnmtI, but not its absence, in post-mitotic neurons protect from ischemic brain injury. NeuroReport 12:3763-3766 (C) 2001 Lippincott Williams & Wilkins.