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RNF10是动脉样硬化保护和调节巨细胞两极分化

Ke-Xin Zhao¹, Shu-Xu Jin², Ming-Hao Li¹

¹Cardiology I, Beidahuang Group General Hospital.

Experimental animals

|December 3, 2025

概括

环指蛋白10 (RNF10) 通过抑制促炎性M1巨细胞和促进抗炎性M2巨细胞,起到抗动脉硬化作用. 这表明RNF10是动脉样硬化的潜在治疗标.

科学领域:

免疫学免疫学免疫学
心血管生物学心血管生物学
分子生物学分子生物学

背景情况:

巨细胞表现出可塑性,分化为促炎M1或抗炎M2表型.
巨细胞极化动态在动脉样硬化的进展中至关重要.
环指蛋白10 (RNF10) 在动脉样硬化期间巨细胞极化中的特定作用需要阐明.

研究的目的:

调查RNF10在调节动脉样硬化背景下的巨细胞极化中的功能.
确定RNF10对M1和M2巨细胞标记物和泡细胞形成的影响.

主要方法:

生成的巨细胞特异性RNF10缺陷的ApoE-/-小鼠 (RNF10^Mac-KO/ApoE^-/-) 和对照 littermates (RNF10^fl/fl/ApoE^-/-) 被养高脂肪饮食.
在体外研究中分离了腹膜巨细胞和使用了RAW264.7小鼠巨细胞.
在巨细胞中通过过度表达载体和小干扰RNA (siRNA) 操纵RNF10表达.
用氧化低密度脂蛋白 (ox-LDL) 刺激巨细胞来诱导泡细胞的形成,并评估M1/M2标记物表达.

主要成果:

与对照小鼠相比,RNF10^Mac-KO/ApoE^-/-小鼠表现出动脉样硬化病变的恶化,居住巨细胞的增加,M1标记物 (iNOS) 表达的增加和M2标记物 (阿基纳-1) 表达的减少.
在巨细胞中RNF10过度表达抑制了M1标记物 (IL-1β,IL-6,iNOS) 和增强了M2标记物 (IL-10,Arg-1).
过度表达RNF10减弱了ox-LDL诱导的泡细胞中的脂质积累,而抑制RNF10则促进了其.

结论:

巨细胞中RNF10缺乏会加剧动脉样硬化,其特征是转向促炎M1表型.
RNF10促进一种抗炎M2巨细胞表型,并减少泡细胞的形成.
巨细胞中的RNF10具有保护性,抗动脉样硬化作用,表明其治疗潜力.

关键词:

RNF10 RNF10是什么意思动脉样硬化动脉样硬化这是一种炎症炎症炎症炎症.巨细胞的两极分化

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