基因组脱甲基酶KDM4B在表观遗传上控制NLRP3的表达,以增强炎症反应
Li Tong1, Hui Song1,2, Yuan Gao1
1Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
基因组脱甲基酶KDM4B通过去除H3K9me3标记来加速NLRP3炎症酶激活,提供了一个新的抗炎点. 高葡萄糖加剧了这一过程,在感染期间恶化了炎症.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- NLRP3炎症酶是炎症和细胞平衡的关键调节者.
- 基因组3氨酸9三甲基化 (H3K9me3) 通常会抑制基因转录.
- H3K9脱甲基化在诱导炎症性细胞因子中的作用尚不清楚.
研究的目的:
- 研究H3K9脱甲基化在NLRP3炎症酶激活中的作用.
- 为了识别参与NLRP3诱导的特定素脱甲基酶.
- 探索KDM4B作为潜在的炎症疾病治疗点.
主要方法:
- 研究KDM4B对Nlrp3促进体H3K9me3脱甲基化的影响.
- 使用Kdm4b缺乏的小鼠和选择性KDM4抑制剂 (ML324).
- 评估了NLRP3炎症酶激活,细胞因子分泌 (IL-1β) 和炎症疾病模型.
- 研究了高葡萄糖水平对KDM4B和NLRP3信号传递的影响.
主要成果:
- KDM4B在Nlrp3促进体中调解H3K9me3脱甲基,诱导NLRP3表达和炎症酶激活.
- KDM4B缺乏和ML324治疗抑制了NLRP3炎症酶激活,并降低了疾病的严重程度.
- 高葡萄糖高调KDM4B,增强NLRP3炎症酶激活和IL-1β分泌,恶化病毒感染相关的炎症.
结论:
- H3K9me3脱甲基化对于通过NLRP3诱导启动炎症至关重要.
- KDM4B作为NLRP3炎症酶激活的表观遗传加速剂.
- 准H3K9me3脱甲基化是一种潜在的抗炎策略.
更多相关视频
10:09Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
Published on: January 26, 2018
09:04Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
相关概念视频
Histone Modification
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
Chromatin Modification in iPS Cells
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
Spreading of Chromatin Modifications
Writers
The writer...
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
