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通过调节miR-31/NF-κB通路,CRNDE可以缓解IL-1β诱导的慢细胞损伤

Jiuxiang Liu¹, Jiangqi Cheng², Hao Zhou²

¹Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University (Jiangsu Province Hospital), No. 300 Guangzhou Road, NanjingJiangsu Province, 210029, China. liujiuxiang@jsph.org.cn.

Journal of orthopaedic surgery and research

|December 20, 2024

概括

长非编码RNACRNDE通过抑制肌肉细胞中的miR-31和NF-κB通路,减少炎症和软骨损伤,从而防止骨关节炎.

科学领域:

生物化学生化学
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

骨关节炎 (OA) 涉及与年龄相关的关节软骨退化.
长非编码RNA的CRNDE与OA病变发生有关.
在OA软骨细胞中,CRNDE的精确机制尚未完全理解.

研究的目的:

研究CRNDE在OA软骨细胞中的作用.
阐明OA中CRNDE的分子机制.
确定CRNDE,miR-31和NF-κB通路之间的关系.

主要方法:

使用介质素 (IL) - 1β刺激的C-28/I2红细胞来模仿OA炎症.
通过RT-PCR评估CRNDE和miR-31表达.
评估了细胞活力,细胞亡,炎症性细胞因子水平 (IL-6,IL-1β,TNF-α),软骨矩阵基因表达 (MMP-13,Aggrecan,COL2A1) 和NF-κB通路激活 (p-p65,p-IκBα).

主要成果:

在OA组织和IL-1β刺激的胆红细胞中,CRNDE的表达减少.
过度表达CRNDE可降低冠状细胞亡,炎症和软骨退化.
在OA组织中,miR-31表达较低,与CRNDE负相关.
miR-31过度表达部分逆转了CRNDE的保护作用.
沉默CRNDE恶化IL-1β诱导的胆细胞损伤,这被NF-κB抑制剂减轻.

结论:

在OA中,CRNDE可减轻IL-1β诱导的状细胞损伤.
通过抑制miR-31介导的NF-κB信号通路来发挥CRNDE的作用.
CRNDE代表了OA治疗的潜在治疗标.

关键词:

在CRNDE中,您可以使用CRNDE.冠状腺细胞 (chondrocyte) 是一种细胞.在 NF-κBB 中.骨关节炎是一种骨关节炎.在 miR-31 里面.

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