DDIT3/CHOP通过抑制髓细胞的抑制促进骨质母细胞中LPS/ATP诱导的烧
Zhipeng Dong1, Beining Yang1, Meie Jia1
1The State 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, China.
Biochimica et biophysica acta. Molecular cell research
|March 23, 2024
概括
炎症会通过内细胞网膜应激诱导骨质质细胞烧灭. DNA损伤诱导转录3 (DDIT3) /CCAAT/增强剂结合蛋白 (C/EBP) 同源蛋白 (CHOP) 通过抑制线粒细胞衰变促进这种作用.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 炎症环境可以诱导内质网膜 (ER) 压力,导致各种细胞类型的热亡.
- DNA损伤诱导转录3 (DDIT3) /CCAAT/增强剂结合蛋白 (C/EBP) 同源蛋白 (CHOP) 是一个关键的ER应激因子,在炎症期间在骨质母细胞上调.
- 在炎症条件下,DDIT3/CHOP在调节骨质细胞烧灭中的作用需要进一步研究.
研究的目的:
- 为了研究DDIT3/CHOP在脂聚糖 (LPS) /腺酸5'-三酸 (ATP) 诱导的骨质细胞烧灭中的作用.
- 阐明涉及PTEN诱导激酶1 (PINK1) /E3泛基素蛋白联酶帕金 (帕金) 介导的基因菌的潜在机制.
主要方法:
- 使用LPS/ATP进行骨质细胞培养和刺激.
- 过度表达了DDIT3/CHOP. 这是一种过度表达.
- 对热灭菌标记物的评估 (NLRP3,卡斯帕-1,GSDMD).
- 使用光成像和西方布洛特的线粒的分析.
- 用碳酸3-基化 (CCCP) 药理学操纵线粒细胞衰变.
主要成果:
- LPS/ATP刺激诱导了骨质母细胞灭,并增加了DDIT3/CHOP的表达.
- DDIT3/CHOP过度表达加剧了热亡,由增加的炎酶激活和热亡执行者水平证明.
- 通过LPS/ATP刺激促进了PINK1/Parkin介导的线粒,而DDIT3/CHOP过度表达则抑制了该过程.
- 通过DDIT3/CHOP过度表达抑制线粒细胞衰变导致热的增加.
- 治疗CCCP可以逆转DDIT3/CHOP对热的作用.
结论:
- 在炎症性环境中,DDIT3/CHOP促进骨质母细胞灭.
- 这种促进通过抑制PINK1/Parkin介导的线粒发生.
- DDIT3/CHOP是一个关键的调节器,通过线性细胞的途径将ER压力与骨质母细胞中的炎结合起来.
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