口腔病原体通过诱导光滑肌肉细胞亡和抑制巨细胞增生抑制动脉样硬化,加剧动脉样硬化
Hanyu Xie1,2,3, Ziyue Qin2,3,4, Ziji Ling1,2,3
1Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, China.
International journal of oral science
|June 28, 2023
概括
Porphyromonas gingivalis 感染引发了光滑肌肉细胞亡,释放了阻碍巨细胞清除并促进动脉样硬化的微RNA. 一种新疗法同时针对牙周炎和动脉样硬化.
科学领域:
- 口腔微生物学和免疫学
- 心血管疾病的研究研究.
- 疾病的分子机制.
背景情况:
- 牙周炎是由 Porphyromonas gingivalis (P. gingivalis) 引起的,增加了动脉样硬化心血管疾病的风险.
- P. gingivalis 诱导亡,但其在斑块形成期间巨细胞清除中的作用尚不清楚.
研究的目的:
- 在光滑肌细胞 (SMC) 和内皮细胞中研究P. gingivalis诱导的亡.
- 阐明细胞亡细胞损害巨细胞增生的机制.
- 评估牙周炎和动脉样硬化的双重治疗策略.
主要方法:
- 通过TLR2激活在SMC和内皮细胞中比较P. gingivalis诱导的亡.
- 分析了感染SMC的细胞外miR-143/145释放及其被巨细胞吸收.
- 评估了miR-143/145对Siglec-G转录和巨细胞发生的影响.
- 利用遗传小鼠模型来确认体内发现的结果.
- 开发并测试了一种使用P. gingivalis预处理的巨细胞膜的纳米粒子疗法.
主要成果:
- SMCs比通过TLR2的内皮细胞更容易受到P. gingivalis诱导的亡.
- 从受感染的SMC释放出的细胞外miR-143/145被巨细胞捕获.
- miR-143/145促进了Siglec-G的转录,抑制了巨细胞的细胞分裂.
- 在活体中,TLR2和miR-143/145在P. gingivalis加速动脉样硬化中起着至关重要的作用.
- 开发的纳米粒子疗法有效地同时治疗了这两种疾病.
结论:
- 牙周杆菌通过miR-143/145颠覆巨细胞功能,导致动脉样硬化.
- 针对TLR2,miR-143/145和Siglec-G提供了一个潜在的治疗途径.
- 一种新的巨细胞膜涂层纳米颗粒显示出治疗同时存在的牙周炎和动脉样硬化的前景.
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