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TUG1通过miR-340-5p介导的PTEN加剧脑缺血-再输液损伤

Fei Li¹, Hui-Kai Zhang¹, Hong-Xiang Jiang¹

¹Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.

Journal of molecular histology

|July 17, 2024

概括

长非编码RNA TUG1通过向miR-340-5p/PTEN通路,使大脑缺血-再输液损伤恶化. 准这一轴为缺血性中风提供了潜在的治疗方法.

科学领域:

分子生物学分子生物学
神经科学是一个神经科学.
遗传学遗传学是一个

背景情况:

长非编码RNAs (LncRNAs) 涉及到大脑缺血-再输液损伤 (CIRI).
在CIRI病原体中LncRNA TUG1的特定作用需要阐明.
了解调节途径对于开发缺血性中风的有效治疗方法至关重要.

研究的目的:

调查LncRNA TUG1加剧CIRI的机制.
确定miR-340-5p/酸酶和张素同类 (PTEN) 途径在TUG1介导的CIRI中的作用.
探索针对TUG1/miR-340-5p/PTEN轴的治疗潜力.

主要方法:

中脑动脉封闭/再输液 (MCAO/R) 的老鼠模型.
在体内给予pcDNA-TUG1和miR-340-5p.
评估神经系统缺陷,心脏病发作大小和分子表达特征 (qRT-PCR,西式涂抹,免疫组织化学).
路西法酶记者测试验证分子相互作用.

主要成果:

在MCAO/R模型中,miR-340-5p降低,TUG1水平增加.
过度表达TUG1会使神经缺陷和心脏病发作大小恶化,而miR-340-5p和agomir则改善了结果.
miR-340-5p直接准TUG1,而TUG1则作为miR-340-5p的竞争性内源RNA (ceRNA),促进PTEN的表达.
TUG1过度表达抑制了miR-340-5p对CIRI的保护作用.

结论:

在LncRNA TUG1中,通过海绵化miR-340-5p和升调PTEN,加剧了CIRI.
在CIRI中,TUG1/miR-340-5p/PTEN监管轴起着至关重要的作用.
针对TUG1/miR-340-5p/PTEN通路是缺血性中风的一种有前途的治疗策略.

关键词:

大脑缺血-再输血损伤缺血性中风是因为缺血性中风.酸酶和张素同类物.氨酸上调的基因1 氨酸上调的基因1 在 miR-340-5p 中使用.

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