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通过NSUN5-介导的m5C修饰,CX3CL1促进M1巨分化和骨质细胞分化

Zhibin Deng¹, Wei Zhong²

¹Department of Orthopedics, Songgang People's Hospital, No.2, Shajiang Road, Songgang Street, Bao'an District, Shenzhen, Guangdong, 518105, China.

Scientific reports

|July 12, 2025

概括

CX3CL1 (Fractalkine) 通过增强M1巨细胞两极分化和骨质细胞分化来促进骨质再吸收. NSUN5通过m5C修饰来调节这一过程,为骨疾病提供潜在的治疗点.

科学领域:

免疫学免疫学免疫学
骨生物学骨生物学骨生物学
分子生物学分子生物学

背景情况:

骨稳定依赖于骨形成和再吸收之间的平衡.
化学因子,如CX3CL1 (Fractalkine),在调节骨质稳定中发挥作用.
了解CX3CL1在骨调节中的分子机制对于治疗骨疾病至关重要.

研究的目的:

研究CX3CL1调节骨质恒温的机制.
阐明NSUN5在CX3CL1介导的骨代谢调节中的作用.
在体内骨质疏松症模型中验证发现.

主要方法:

qPCR和西部涂抹来评估CX3CL1的表达.
通过shRNA介导的CX3CL1/NSUN5.5的淘汰和过度表达.
分析促炎因素,M1/M2标志物,骨质细胞活动和关键骨质细胞生成因子.
机械验证的MeRIP,RIP和双路西法酶记者试验.
卵巢切除术 (OVX) 诱导的骨质疏松症小鼠模型用于体内研究.

主要成果:

在LPS和RANKL刺激的巨细胞中,CX3CL1的表达增加.
CX3CL1敲击抑制了M1极化和骨质细胞分化.
通过m5C修饰,NSUN5抑制了CX3CL1的稳定性.
过度表达CX3CL1逆转了NSUN5的抑制作用.
在OVX小鼠中,NSUN5保留了骨质,但与CX3CL1的联合表达取消了这种效应.

结论:

CX3CL1加速M1巨细胞极化和骨质细胞分化.
NSUN5通过m5C修饰来调节CX3CL1的稳定性.
这种相互作用为骨质平衡和相关疾病提供了新的治疗点.

关键词:

骨平衡骨的平衡骨的平衡在CX3CL1中.在M1极化中,M1极化这是NSUN5的5号.骨质细胞分化差异化

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