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LncRNA THUMPD3-AS1通过miR-485-5p和ARHGAP8调节精神分裂症中的行为和突触结构异常
Xiaojuan Gong1,2,3, Lingxi Chen4,5, Xin Guo6
1College of Medicine and Forensic, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|October 31, 2025
概括
一个涉及THUMPD3-AS1,miR-485-5p和ARHGAP8的新型非编码RNA通路调节了精神分裂症 (SCZ) 中的突触功能. 这一轴影响着actin重塑和突触缺陷,提供潜在的治疗点.
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:
- 精神分裂症 (SCZ) 涉及突触结构缺陷,但非编码RNAs (ncRNAs) 的作用尚不清楚.
- 了解ncRNA失调对于阐明SCZ病变发生至关重要.
研究的目的:
- 确定和描述NCRNA调节网络驱动SCZ中的突触异常.
- 研究THUMPD3-AS1/miR-485-5p/ARHGAP8轴在突触功能和SCZ病理中的作用.
主要方法:
- 使用ceRNAxis对SCZ转录组,GWAS数据和表达特征进行综合分析.
- 在体外和体内 (老鼠模型) 的功能验证.
- 在人类和小鼠组织中进行跨物种验证.
主要成果:
- 确定THUMPD3-AS1/miR-485-5p/ARHGAP8轴是突触功能的一个关键调节器.
- THUMPD3-AS1封存miR-485-5p,缓解ARHGAP8的抑制,ARHGAP8通过RhoB/C.非正规地激活ROCK2,而ROCK2则通过RhoB/C.进行非正规激活.
- 这一途径破坏了actin重塑,导致不成熟的树突和突触缺陷,模仿SCZ病理.
结论:
- 一个新的ncRNA驱动的致病级联涉及非正规的RhoB/C-ROCK2信号,是SCZ突触破坏的基础.
- 针对这一轴为SCZ提供了潜在的治疗策略.
- 这些发现突出了SCZ病变的跨物种保存机制.
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