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缺氧预条件通过调节DNA甲基化 in vitro 和 in vivo 增加了 Notch1 的活性

Zhehan Chang^1,2,3, Qi Liu⁴, Peijia Fan⁵

¹Center for Translational Medicine, The Third People's Hospital of Longgang District, Shenzhen, China.

Molecular biology reports

|April 15, 2024

概括

缺氧预条件 (HPC) 增强了小鼠的空间记忆和海马神经发生. 这种神经保护与Notch1信号通路的激活和Notch1基因的DNA甲基化减少有关.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

以前的研究表明,低氧预条件 (HPC) 改善了成年小鼠的空间学习和记忆.
成年海马神经发生对于学习和记忆至关重要.
诺奇通路与神经发生和认知功能有关,但其在通过DNA甲基化诱导HPC的神经再生中的作用尚不清楚.

研究的目的:

调查Notch路径是否通过在缺氧预条件 (HPC) 后的DNA甲基化变化来调节海马神经再生.

主要方法:

通过重复的缺氧暴露,建立了HPC小鼠和HT22细胞模型.
使用下一步测试评估空间学习.
通过实时PCR和Western blot进行量化Notch1和HES1表达 (mRNA和蛋白质).
通过使用共聚焦显微镜在海马中计数BrdU阳性细胞和Notch1表达来检查神经发生.
使用甲基化特异性PCR (MS-PCR) 分析了Notch1促进体DNA甲基化.

主要成果:

在降级测试中,HPC显著提高了性能.
HPC增加了Notch1和HES1mRNA和蛋白质水平.
HPC增加了BrdU阳性细胞的数量和海马牙状回形中Notch1的表达.
HPC显著降低了Notch1促进体的DNA甲基化水平.
用HT22细胞进行的体外研究反映了体外发现.

结论:

通过激活Notch1信号通路,HPC提供神经保护.
HPC对Notch1信号的激活涉及对其DNA甲基化状态的调节.
这些分子变化促进海马神经元再生,增强认知功能.

关键词:

通过DNA甲基化.缺氧预先调节的预先条件学习和记忆的学习和记忆神经新生是神经发生的过程.标记1 标记1 标记

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