Meis1通过调控胚胎大脑的细胞增殖能力在皮质发育中发挥作用。

IF 1.3 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL Biomedical Research-tokyo Pub Date : 2022-01-01 DOI:10.2220/biomedres.43.91
Eriko Isogai, Kazuhiro Okumura, Megumi Saito, Yurika Tokunaga, Yuichi Wakabayashi
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引用次数: 3

摘要

Meis1(髓系亲生态插入位点1)与胚胎发育和癌症有关。在本研究中,为了分析Meis1在神经干细胞中的功能,我们将Meis1fl/fl (Meis1 floxed)小鼠与nesting - cre小鼠杂交。结果显示,meis1条件敲除小鼠出现大脑皮质畸形。这些小鼠的皮质明显比野生型小鼠薄。在E14.5时,与野生型胚胎相比,Meis1基因敲除胚胎的大脑皮层中BrdU掺入和pax6阳性的放射状胶质细胞显著减少,而tbr2阳性的中间祖细胞和neun阳性的分化神经元则没有明显减少。用cleaved caspase3抗体免疫染色检测细胞死亡,结果显示敲除胚胎与野生型胚胎皮层无差异。此外,通过子宫内电穿孔敲除胚胎中的Meis1表明细胞迁移在皮质发育过程中受到干扰。因此,Meis1可能通过调控胚胎大脑皮层细胞的增殖和迁移,在皮层发育过程中发挥重要作用。
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Meis1 plays roles in cortical development through regulation of cellular proliferative capacity in the embryonic cerebrum.

Meis1 (myeloid ecotropic insertion site 1) is known to be related to embryonic development and cancer. In this study, to analyze the function of Meis1 in neural stem cells, we crossed Meis1fl/fl (Meis1 floxed) mice with Nestin-Cre mice. The results showed that Meis1-conditional knockout mice showed cerebral cortex malformation. The mice had a significantly thinner cortex than wildtype mice. At E14.5, BrdU incorporation and Pax6-positive radial glial cells were significantly decreased in the cerebral cortex of Meis1 knockout embryos as compared with wild-type embryos, whereas Tbr2-positive intermediate progenitors and NeuN-positive differentiated neurons were not. Cell death detected by immunostaining with cleaved caspase3 antibody showed no difference in the cortex between knockout and wild-type embryos. Furthermore, knockout of Meis1 in embryo by in utero electroporation showed that cellular migration was disturbed during cortical development. Therefore, Meis1 could play important roles during cortical development through the regulation of cell proliferation and migration in the embryonic cerebral cortex.

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来源期刊
Biomedical Research-tokyo
Biomedical Research-tokyo 医学-医学:研究与实验
CiteScore
2.40
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..
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