高葡萄糖通过GSDME O-GlcNAcylation促进脂聚糖诱导的巨细胞灭
1Department of Stomatology, Inner Mongolia Autonomous Region People's Hospital, Hohhot City, Inner Mongolia, China.
Journal of periodontal research
|September 25, 2024
概括
高葡萄糖通过增加GSDME的O-GlcNAcylation来促进糖尿病牙周炎中的巨细胞灭. 这一发现为牙周炎治疗提供了潜在的新治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 糖尿病牙周炎涉及高葡萄糖 (HG) 损害牙周组织.
- 巨质炎与牙周炎的严重程度相关.
- O-GlcNAcylation与牙周炎的发病有关,但其在HG诱导的巨细胞灭中的作用尚不清楚.
研究的目的:
- 为了研究HG对巨细胞中GSDME的O-GlcNAcylation的影响,GSDME是一种烧亡调节剂.
- 阐明在糖尿病牙周炎中连接HG,O-GlcNAcylation和巨炎的机制.
主要方法:
- 从糖尿病牙周炎患者收集血液.
- 将THP-1单细胞分化为巨细胞,并以HG在体外处理.
- 通过qPCR测量了GSDME表达.
- 通过细胞活力,细胞毒性和炎症标志物评估热.
- 分析了GSDME O-GlcNAcylation使用共免疫沉和西部斑点.
主要成果:
- HG提高了GSDME的表达,并促进了巨细胞的灭 (增加了IL-1β,IL-18,TNF-α,NLRP3,GSDMD,Caspase-1).
- HG增加了GSDME O-GlcNAcylation,在Ser339部位中介于OGT.
- OGT敲击抑制了HG诱导的热,GSDME过度表达部分逆转了这种效应.
结论:
- HG增强了OGT介导的GSDME O-GlcNAcylation,从而增加了巨细胞中的热亡.
- 这些发现表明,针对牙周炎的新治疗策略是针对这种途径.
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