在内皮细胞中,RhoA/ROCK1通过Porphyromonas gingivalis诱导的Drp1调节线粒体功能障碍
Qin Dong1, Yuxiao Luo1, Yuqing Yin1
1Department of Periodontics, School of Stomatology, China Medical University, Shenyang, China.
Journal of cellular and molecular medicine
|June 6, 2023
概括
葡萄牙炎感染会通过RhoA/ROCK1通路引起内皮细胞线粒体功能障碍. 这条通路调节了Drp1的酸化和转位,为牙周炎相关的内皮功能障碍提供了一个新的治疗点.
科学领域:
- 细胞生物学 细胞生物学
- 病原体研究 病原体研究
- 血管生物学 血管生物学
背景情况:
- Porphyromonas gingivalis 是牙周炎的一个关键病原体.
- 由P. gingivalis诱导的内皮线粒体功能障碍涉及Drp1,但上游信号通路尚不清楚.
研究的目的:
- 研究RhoA/ROCK1通路在P. gingivalis诱导的内皮细胞中的线粒体功能障碍中的作用.
主要方法:
- 在EA.hy926内皮细胞感染P. gingivalis.
- 评估RhoA/ROCK1通路的激活,使用西方抹黑和拉下测试.
- 评估线粒体形态,功能 (ATP,mtDNA,孔隙开放性) 和Drp1酸化/转移.
- 利用RhoA和ROCK1抑制剂来确定途径的参与.
主要成果:
- 牙周杆菌感染激活了RhoA/ROCK1通路,并在内皮细胞中诱导了线粒体功能障碍.
- 抑制RhoA或ROCK1部分改善了P. gingivalis诱导的线粒体功能障碍.
- 抑制RhoA/ROCK1阻断了P. gingivalis诱导的Drp1酸化和线粒体转位.
结论:
- 在RhoA/ROCK1通路中介于P. gingivalis诱导的内皮线粒体功能障碍.
- 这条通路调节了Drp1的酸化和转位,揭示了P. gingivalis诱导的内皮功能障碍的新机制.
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