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ROS诱导的牙纤维细胞衰老:在牙周疾病中加剧炎症反应的含义

Shuling Guo¹, Liangliang Fu¹, Chenghu Yin¹

¹State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, 430079, China.

|April 17, 2024

概括

牙纤维细胞中的细胞衰老通过增加炎症驱动牙周病. 氧化应激导致这种衰老,导致释放激活免疫细胞的因素,如中性粒细胞和巨细胞.

科学领域:

口腔生物学口腔生物学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

牙周病涉及牙周组织的慢性炎症.
细胞衰老与慢性炎症有关,但其在牙周病中的作用尚不清楚.

研究的目的:

研究细胞衰老在牙周病病原发生中的作用和机制.
识别细胞衰老标志物及其对牙纤维细胞的影响.

主要方法:

炎症的牙组织的单细胞RNA测序.
人类牙纤维细胞 (H-GF和I-GF) 的分离和表征.
对衰老标记物 (SA-β-gal,p16INK4A),氧化应激 (ROS),DNA损伤,细胞活性和基因表达 (SASP因子) 的检测.
对中性粒细胞外细胞陷 (NET) 形成和巨细胞两极分化的超效应的评估.

主要成果:

在炎症的牙组织中的纤维细胞和内皮细胞中观察到高调的细胞衰老.
炎症的牙纤维细胞 (I-GFs) 显示SA-β-gal增加,形态扩大和p16INK4A表达.
I-GFs表现出增加的ROS,线粒体ROS和DNA损伤,由NAC可逆.
I-GFs表现出减少的迁移/扩散,但增加了SASP因子 (IL-1β,IL-6,TGF-β,IL-8).
I-GF超剂增强了NET的形成,并促进了M1巨细胞的两极分化.

结论:

氧化应激诱导的DNA和线粒体损伤导致炎症的牙中人类牙纤维细胞的细胞衰老.
衰老的纤维细胞分泌SASP因子,激活中性粒细胞和巨细胞,导致牙周炎症.

关键词:

细胞衰老细胞衰老人类牙纤维细胞.巨细胞的两极分化中性粒细胞外细胞陷牙周疾病牙周疾病与衰老相关的分泌表现型

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