由ITE向的H3K9乙化-NF-κB-AP-1结局限制TNF-α诱导的MMP-9表达在单细胞中
Fatemah Bahman1, Shihab Kochumon1, Md Zubbair Malik2
1Immunology and Microbiology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.
Journal of immunology (Baltimore, Md. : 1950)
|September 27, 2025
概括
印-3-碳-醇-4-碳酸甲基 (ITE) 抑制瘤缩因子-α (TNF-α) 诱导的矩阵金属蛋白酶9 (MMP-9) 表达. 这通过MMP-9基因促进者的表观遗传调节发生,为炎症性疾病提供了潜在的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 矩阵金属蛋白酶9 (MMP-9) 在炎症性疾病的发病过程中至关重要,并由TNF-α上调调节.
- 印-3-碳-醇-4-碳酸甲基 (ITE) 是一种内源性酸碳水化合物受体结合体,参与炎症.
- ITE对单细胞中TNF-α诱导的MMP-9表达的作用尚不清楚.
研究的目的:
- 研究ITE对单细胞细胞中TNF-α诱导的MMP-9表达的作用.
- 阐明ITE作用的潜在分子机制.
主要方法:
- 用ITE预处理了THP-1单细胞和原发性人体单细胞.
- 在mRNA和蛋白质水平上评估TNF-α诱导的MMP-9表达.
- 分析了表观遗传修饰 (H3K9乙化),转录因子结合 (NF-κB,AP-1) 和基因表达.
主要成果:
- 在两种细胞类型中,ITE预处理显著抑制了TNF-α诱导的MMP-9表达.
- ITE抑制了炎症基因表达,并降低了MMP-9促进体的H3K9乙化.
- ITE抑制了TNF-α诱导的NF-κB和AP-1与MMP-9促进体的结合.
结论:
- 通过H3K9乙化/NF-κB/AP-1信号轴的表观遗传调制,ITE有效地降低了TNF-α诱导的MMP-9表达.
- ITE的机制涉及抑制炎症途径和转录因子结合.
- ITE具有缓解MMP-9相关炎症疾病的潜在治疗剂.
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