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沉默STUB1通过诱导NRF2-介导的M2巨细胞极化来缓解骨关节炎

Nan Cao¹, Danni Wang¹, Bin Liu¹

¹Department of Orthopedics, General Hospital of Northern Theater Command, Shenyang 110016, Liaoning Province, China.

Molecular immunology

|November 22, 2023

概括

沉默STUB1将巨细胞转移到抗炎M2状态,通过抑制NRF2无处不在,缓解骨关节炎的进展和损伤. 这一发现为骨关节炎治疗提供了新的治疗点.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
生物化学生物化学

背景情况:

骨关节炎 (OA) 的发病包括由亲炎性M1巨细胞驱动的慢性炎症.
将巨细胞转移到抗炎M2表型是OA的一种有前途的治疗策略.
在OA中调节巨细胞极化的精确分子机制尚未完全理解.

研究的目的:

在OA的背景下,研究STUB1 (一种E3泛基因酶) 在巨细胞极化中的作用.
阐明STUB1影响OA病理的潜在分子机制.

主要方法:

建立了OA的体内大鼠模型和体内脂聚糖 (LPS) 诱导的淋巴细胞模型.
评估了组织病理学变化,巨细胞两极分化 (M1/M2) 和炎症标志物 (TNF-α,IL-6).
利用共同免疫沉 (CO-IP) 和拉下测试来确定STUB1-NRF2相互作用和无处不在.

主要成果:

沉默STUB1显著缓解了老鼠的OA症状,减少了炎症和组织损伤.
STUB1 knockdown促进了M2巨细胞的两极分化,并在体内和体外抑制了M1巨细胞.
STUB1直接无处不在NRF2,NRF2对于STUB1对M2极化的影响至关重要. 沉默STUB1提高了NRF2的调节,增强了状细胞的活力,减少了亡.

结论:

抑制STUB1通过抑制NRF2的无化促进了M2巨细胞的两极分化,从而减轻了OA.
向STUB1代表了通过调节巨细胞表型来管理骨关节炎的潜在治疗方法.

关键词:

巨细胞的两极分化这就是NRF2的NRF2.骨关节炎是一种骨关节炎.一个是STUB1一个是STUB1.在Ubiquitination中使用.

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