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由lncRNA-NONMMUT020270.2调节的ITPR2的表达在LPS刺激的HT22细胞中

Lan Liu^1,2, Liang Tang³, Yan Wang³

¹Medical College, Tibet University, Lhasa, Tibet, 850000, People's Republic of China.

|July 23, 2024

概括

长非编码RNANONMMUT020270.2积极调节异醇1,4,5-三酸盐受体2型 (ITPR2) 的表达. 这两种分子的下调促进了类似阿尔茨海默病的病理,包括细胞亡和水平的增加.

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
遗传学是一个遗传学.

背景情况:

阿尔茨海默病 (AD) 与改变的长非编码RNA (lncRNA) 表达相关.
在AD小鼠海马体中,lncRNA NONMMUT020270.2是向下调节的,并与伊诺西托1,4,5-三酸盐受体2型 (ITPR2) 共同表达.
在AD病变发生过程中,lncRNA-NONMMUT020270.2和ITPR2之间的调控关系尚不清楚.

研究的目的:

调查 lncRNA-NONMMUT020270.2 和 ITPR2.2 之间的监管关系.
确定lncRNA-NONMMUT020270.2在类似阿尔茨海默病的细胞反应中的作用.

主要方法:

通过 lncRNA-NONMMUT020270.2 过度表达或沉默载体感染HT22细胞.
用脂聚糖 (LPS) 刺激细胞诱导AD类病理.
使用定量PCR,ELISA,西部涂抹,霍希斯特染色和流动细胞测量来评估基因和蛋白质表达,细胞活力,细胞亡和细胞内水平.

主要成果:

在LPS刺激下降了细胞活力和ITPR2表达,同时增加了p-tau,Aβ1-42,亡和细胞内.
lncRNA-NONMMUT020270.2过度表达上调了ITPR2和IP3R,抑制了p-tau和Aβ1-42,减少了细胞亡,并降低了细胞内.
lncRNA-NONMMUT020270.2沉默具有相反的效果,降低ITPR2和IP3R的调节,并加剧了类似AD的病理.

结论:

lncRNA-NONMMUT020270.2与LPS诱导细胞中的ITPR2表达具有正相关性.
对lncRNA-NONMMUT020270.2和ITPR2的下调可能会促进细胞亡,增加细胞内的度,从而导致AD的发病.

关键词:

阿尔茨海默氏症的疾病是阿尔茨海默氏症.细胞灭亡 (apoptosis) 是一种死亡的过程.在Ca2+中.在ITPR2中使用ITPR2.长长的非编码RNAs.

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