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17β-雌二醇抑制了小鼠巨细胞系RAW 264.7中的Notch1激活

Paolo Severi¹, Alessia Ascierto¹, Luisa Marracino¹

¹Department of Translational Medicine and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, 44124, Italy.

Molecular biology reports

|November 8, 2024

概括

17β-雌激醇 (E2) 抑制了巨细胞中的Notch1激活,减少了由脂聚糖 (LPS) 和干扰素- (IFNγ) 诱导的促炎M1表型. 这项研究揭示了巨细胞中一种新的Notch1-雌激素受体α (ERα) 相互作用,这表明炎症性疾病的潜在治疗点.

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:

巨细胞是免疫反应和炎症的关键调节者.
亲炎性M1表型是由托尔类受体4 (TLR4) 和干扰素- (IFNγ) 信号诱导的,激活了Notch通路.
17β-雌二醇 (E2) 可以减少LPS介导的炎症,但其对巨细胞中Notch1的影响尚不清楚.

研究的目的:

调查E2对LPS/IFNγ刺激的巨细胞中Notch1激活的E2的影响.
探索Notch通路与巨细胞中的雌激素受体α (ERα) 之间的相互作用.
确定针对Notch1用于管理炎症性疾病的潜力.

主要方法:

使用LPS/IFNγ,E2和一个Notch抑制剂 (DAPT) 治疗RAW 264.7巨细胞.
使用定量PCR和西方抹杀来评估iNOS,Notch路径组件和MAPK信号.
分析了p38酸化作为E2作用的机制.

主要成果:

E2减少了LPS/IFNγ诱导的Notch1激活,部分是通过抑制p38酸化.
诺奇1抑制导致雌激素受体α (ERα) 的蛋白质水平增加.
在巨细胞中发现了一种新的Notch1-ERα相互作用.

结论:

通过抑制Notch1.1,E2可能会减弱M1亲炎性巨细胞表型.
这些发现表明,巨细胞中Notch1和ERα之间存在相互调节.
针对Notch1可能为与炎症相关的疾病提供新的治疗策略.

关键词:

17β-雌二醇是17β-雌二醇中的一种.炎症炎症是一种炎症.巨细胞是一个巨细胞.口路径是一个口路径.

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