在THP-1单细胞中IL-1β诱导的CXCL10表达涉及JNK/c-Jun和NF-κB介导的信号传递
Shihab Kochumon1, Amnah Al-Sayyar2, Texy Jacob1
1Immunology & Microbiology Department, Dasman Diabetes Institute, Dasman 15462, Kuwait.
Pharmaceuticals (Basel, Switzerland)
|July 27, 2024
概括
介质素-1β (IL-1β) 刺激单细胞细胞中C-X-C动机化学因子连接体10 (CXCL10) 的产生. 这个过程涉及JNK/c-Jun/NF-κB信号通路,对于炎症反应至关重要.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- CXCL10 (IP-10) 与肥胖和2型糖尿病等炎症性疾病有关.
- IL-1β是一种关键的促炎性细胞因子,在代谢性炎症中升级调节.
研究的目的:
- 为了确定IL-1β是否诱导单细胞中CXCL10的表达.
- 为了研究这种诱导的潜在分子机制.
主要方法:
- 人类单细胞THP-1细胞被IL-1β刺激.
- 使用RT-PCR和ELISA量化CXCL10基因和蛋白质的表达.
- 信号通路通过西式涂抹,抑制剂和siRNA进行分析.
主要成果:
- IL-1β显著增加了单细胞细胞中的CXCL10mRNA和蛋白质水平.
- 只有JNK抑制抑制了IL-1β诱导的CXCL10表达;MEK/ERK和p38 MAPK抑制剂没有影响.
- CXCL10的诱导依赖于JNK/c-Jun和NF-κB的信号传递.
结论:
- 刺激IL-1β会诱导单细胞中CXCL10的表达.
- 在JNK/c-Jun/NF-κB信号轴中介于这种IL-1β诱导的CXCL10表达.
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