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在miR-29-3p家族抑制炎症性骨解

Bongjin Shin¹, Henry C Hrdlicka², Sangita Karki²

¹Center on Aging, UConn Health, Farmington, Connecticut, USA.

Journal of cellular physiology

|May 20, 2024

概括

微RNA-29-3p通过向TNF受体1来抑制炎症性骨质细胞形成. 降低miR-29-3p活性增强了TNF-α诱导的骨质损失,表明了治疗潜力.

科学领域:

骨生物学与炎症骨生物学与炎症
微型RNA规则微型RNA规则
类风湿性关节炎的发病原因

背景情况:

骨质细胞驱动炎症诱导的骨损失,在类风湿性关节炎中至关重要.
微RNA-29-3p家族成员促进RANKL诱导的骨质细胞功能.
在TNF-α诱导的骨质细胞形成中,miR-29-3p的作用尚不清楚.

研究的目的:

研究miR-29-3p在TNF-α诱导的骨质结晶生成中的作用.
确定miR-29-3p是否影响髓状细胞系的承诺.
探索miR-29-3p作为炎症性骨损失的治疗点.

主要方法:

使用了大量的RNA-seq,组织学,qRT-PCR,记者检测和西部斑.
雇佣了特定于骨髓细胞的miR-29-3p敲除小鼠 (LysM-cre).
检查了骨髓单细胞细胞培养和体内骨质溶解模型.

主要成果:

miR-29-3p的淘汰促进了骨髓状细胞中高细胞动力学/促炎性基因特征.
减少的miR-29-3p活性在体外和体内突显了TNF-α诱导的骨质细胞形成.
miR-29-3p直接准TNF受体1 (TNFR1),调节TNF-α信号传递的灵敏度.
miR-29-3p似乎抑制了巨细胞系的结合,并抑制了炎症性骨质细胞生成.

结论:

miR-29-3p在骨质平衡中表现出性作用,促进RANKL诱导的骨质细胞活性,同时抑制TNF-α诱导的骨质细胞生成.
miR-29-3p knockdown 启动了髓状细胞的炎症反应,并可能将血统承诺转移到巨细胞.
miR-29-3p家族代表了调节炎症反应和骨损失的潜在治疗标.

关键词:

排名连接体的连接体.骨头骨头骨头骨头巨细胞是一个巨细胞.这是一个微型RNA.骨质结晶体的骨质细胞.瘤丧亡因子α因子

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