N6 - - 甲基氨酸甲基转移酶METTL14与类风湿性关节炎中的巨细胞两极分化有关
Ziheng Zhu1, Lei Wan1,2
1Department of Rheumatology and Immunology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui 230031, P.R. China.
Experimental and therapeutic medicine
|August 8, 2024
概括
甲基转移酶14 (METTL14) 在类风湿性关节炎 (RA) 患者中升高,与疾病严重程度和炎症相关. 通过MAPK通路促进巨细胞极化,METTL14可能会使RA恶化.
科学领域:
- 免疫学 免疫学 免疫学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 分子生物学分子生物学
背景情况:
- 类风湿性关节炎 (RA) 的发病包括由巨细胞两极分化驱动的炎症反应.
- N6-甲基氨酸 (m6A) RNA甲基化是一种影响巨细胞两极分化的表观遗传修饰.
- 对于m6A甲基化在RA巨分化中的确切作用尚不清楚.
研究的目的:
- 研究m6A甲基化,特别是甲基转移酶14 (METTL14) 的功能和机制,在RA的背景下研究巨细胞极化.
- 确定METTL14表达与RA临床和炎症标志物之间的相关性.
主要方法:
- 反转录定量PCR (RT-qPCR) 来评估m6A甲基酶基因和信号通路组件的mRNA表达.
- 对METTL14蛋白水平的西部斑点分析.
- 针对细胞分泌因子和巨细胞标记物的ELISA和流细胞计 (CD68+,CD86+).
- 基因和基因组的京都百科全书 (KEGG) 途径分析.
主要成果:
- 在RA患者的外周血液和突组织中观察到METTL14表达的升高.
- METTL14水平与C反应蛋白,类风湿因子和促炎性细胞因子TNF-α正相关.
- METTL14表达与M1巨标记物 (CD68+,CD86+) 相关,并预测了视觉模拟尺度得分.
- METTL14与MAPK信号通路有关,在高METTL14组中增加了JNK和ERK2表达.
结论:
- 在RA中,METTL14是上调调的,与疾病严重程度和炎症标志物有关.
- 通过MAPK信号通路促进巨细胞极化,METTL14可能会加剧RA.
- METTL14代表了管理RA相关炎症的潜在治疗标.
相关概念视频
T Cell Types and Functions
966
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
966
The JAK-STAT Signaling Pathway
8.7K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
8.7K


