阻断长非编码RNA BISPR 减弱了人类微质中促炎性细胞因子IL-6的产生

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Yingying Wang¹, Xiaoyu Zhang², Shengqiu Li²

¹Hebei Key Laboratory of Nerve Injury and Repair, Chengde Medical University, Chengde, 067000, China; Laboratory of Gene Engineering and Genomics, School of Basic Medical Sciences, Chengde Medical University, 067000, Chengde, China.

Biochemical and biophysical research communications

|November 23, 2025

概括

长非编码RNA BISPR通过增强STAT1激活来放大微质炎症,独立于TLR4通路. 这一发现凸显了BISPR作为神经炎症疾病的潜在治疗点.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

慢性微质炎症与神经退行性疾病有关.
长非编码RNA BISPR在微质炎症中的作用目前尚不清楚.
干扰素 (IFN) 在各种细胞类型中诱导BISPR表达.

研究的目的:

研究 lncRNA BISPR 在调节微质炎症反应中的作用.
探索BISPR作为神经炎症的潜在治疗点.

主要方法:

用RT-qPCR测量HMC3微质中用IFN-γ,IFN-α 2b或TNF-α刺激的IncRNA BISPR表达.
建立一个BISPR-knockdown (BISPR-KD) HMC3微质细胞系.
RNA测序 (RNA-seq) 用于分析BISPR-KD细胞中的转录基因变异.
西方斑点用于评估IL-6,TLR4,STAT1和酸化STAT1 (p-STAT1) 的蛋白质水平.

主要成果:

BISPR表达显著受到IFN-γ,IFN-α 2b和TNF-α的诱导.
通过BISPR敲除抑制的脂聚糖 (LPS) 或LPS/IFN-γ诱导的IL-6表达.
转录组分析揭示了在炎症反应和JAK-STAT信号通路中差异表达基因的丰富.
在不影响TLR4路径组件的情况下,BISPR敲击降低了在氨酸701的STAT1酸化.

结论:

lncRNA BISPR作为微质炎症的关键积极调节者.
BISPR的功能并非通过TLR4通路进行介导.
BISPR可能会强化STAT1激活,在JAK-STAT1信号通路中创建一个积极的反循环,以放大炎症反应.
BISPR是微质中的过度神经炎症的潜在治疗点.

关键词:

在IL-6的研究中,IL-6被认为是IL-6的基因.微质细胞中的微质细胞神经炎症是一种神经炎症.美国国家统计局 (STAT1)在cRNA BISPR 中.

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