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长非编码RNA SNHG8驱动压力颗粒的形成在陶氏病变

Reshma Bhagat¹, Miguel A Minaya¹, Arun Renganathan¹

¹Department of Psychiatry, Washington University in St Louis, St Louis, MO, USA.

Molecular psychiatry

|September 21, 2023

概括

长非编码RNAs (lncRNAs) 与病有关. 减少SNHG8表达与病理和压力颗粒形成有关,这表明它在神经退行症中起因作用.

科学领域:

神经科学是一个神经科学.
遗传学是一个遗传学.
分子生物学分子生物学

背景情况:

病是一种神经退行性疾病,与蛋白聚合有关.
MAPT基因突变会导致一些病,但下游效应尚不清楚.
长非编码RNAs (lncRNAs) 调节基因表达,可能在病症中发挥作用.

研究的目的:

研究 lncRNAs 在 MAPT 突变驱动的病变中的作用.
确定在病症中失调的特定 lncRNAs.
确定lncRNAs,tau和压力颗粒形成之间的功能关系.

主要方法:

使用患者衍生干细胞神经元与MAPT突变 (P301L,IVS10 + 16,R406W) 和CRISPR纠正的对照.
进行了转录组分析,以识别差异表达的 lncRNAs.
研究了lncRNAs,tau和RNA结合蛋白之间的相互作用 (例如,TIA1).
评估了SNHG8操纵在体外和患者衍生神经元中的压力颗粒形成的影响.

主要成果:

在三个MAPT突变中发现了15个常见的 lncRNAs.
在MAPT突变神经元中,SNHG8显著减少,这是小鼠病症模型,以及人类FTLD-tau,PSP和AD大脑.
SNHG8与tau和TIA1相互作用;突变的tau过度表达减少了SNHG8和增加了压力颗粒.
恢复SNHG8表达减少了压力颗粒的形成和TIA1水平.

结论:

SNHG8的失调是病的潜在因果因素.
在MAPT相关的神经退行症中,SNHG8的减少有助于通过TIA1形成压力颗粒.
lncRNAs代表了病的新型治疗标.

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