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通过阻断NLRP3炎症酶激活,FoxO1 knockdown抑制了RANKL诱导的骨质结晶形成

Zhanqi Wang^1,2, Wenxin Luo¹, Guorui Zhang¹

¹State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

|November 6, 2023

概括

叉头转录因子O1 (FoxO1) 在牙周炎期间在骨质细胞中得到丰富. FoxO1 knockdown通过抑制NF-κB和NLRP3炎症酶通路来抑制骨质细胞的形成,为牙周炎提供了潜在的治疗标.

科学领域:

口腔生物学和疾病
骨再吸收的细胞和分子机制
炎症和免疫学炎症和免疫学

背景情况:

牙周炎涉及由骨质细胞活动驱动的显著膜骨损失.
特定的转录因子,如叉转录因子O1 (FoxO1) 在牙周炎期间骨质细胞形成中的作用需要进一步阐明.
了解调节骨质细胞形成的分子通路对于开发向疗法至关重要.

研究的目的:

为了研究骨质结晶性FoxO1和牙周炎之间的关联.
探索FoxO1倒置影响骨质细胞形成和分化的机制.
根据FoxO1的作用,确定牙周炎的潜在治疗点.

主要方法:

在老鼠中建立了一种由带诱导的牙周炎模型.
使用免疫光染色来检测骨质细胞FoxO1.1.
进行了RNA测序 (RNA-seq) 以探索机制,并补充了西部涂抹,qPCR和ELISA.
用MCC950作为NLRP3炎症酶抑制剂,以评估其对骨质细胞形成的影响.

主要成果:

在牙周炎模型的膜骨中发现骨质类FoxO1被丰富了.
FoxO1的淘汰导致骨质细胞形成受损,其特点是与差异化相关的基因的表达减少和不完全成熟.
RNA-seq分析表明,FoxO1 knockdown抑制了核因子kappa B (NF-κB) 和NLRP3炎症体信号通路.
使用MCC950抑制NLRP3炎症酶显著降低了骨质细胞形成.

结论:

通过抑制NF-κB信号和NLRP3炎症酶激活,FoxO1 Knockdown可以抑制骨质细胞形成.
这项研究强调了FoxO1在调节牙周炎期间骨质细胞形成中的关键作用.
准FoxO1是一个有前途的治疗策略来治疗牙周炎.

关键词:

在 NF-κB 信号传输中.有关RNA测序的RNA测序叉头转录因子的转录因子炎症酶体 (inflammasomes) 是一种炎症酶体.骨质细胞的骨质细胞.牙周炎是指牙周炎的一种疾病.

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