循环RNA circFNDC3B 在克罗恩病中调节M2巨细胞激活和肠道炎症
Juan Yin1,2, Mengyao Liu1, Liping Zhang1
1Center for IBD Research and Department of Gastroenterology, Suzhou Municipal Hospital Affiliated to Nanjing Medical University, Suzhou, China.
循环RNAcircFNDC3B在克罗恩病 (CD) 患者中升高,通过circFNDC3B-HuR-FNDC3B-TGFβ通路促进M2巨细胞激活和单细胞粘附,为炎症性肠病 (IBD) 机制提供了新的见解.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 胃肠病学 胃肠病学
背景情况:
- 克罗恩氏病 (CD) 的发病包括单细胞-巨细胞功能障碍,但循环RNA_103516 (circFNDC3B) 的作用尚不清楚.
- 在CD患者的外周血液单细胞和炎症性粘膜中,circFNDC3B的表达很高.
研究的目的:
- 研究circFNDC3B在调节单细胞-巨细胞分化和CD中的功能中的作用.
- 阐明 circFNDC3B 在 CD 病原发生过程中的作用背后的分子机制.
主要方法:
- 定量实时PCR和FISH用于分析circFNDC3B表达.
- 为了确定调节机制,进行RNA测序,RNA免疫沉降 (RIP) 和RNA拉下测试.
- 在体外测试包括细胞活力,细胞化,分化和粘附测试.
主要成果:
- 在CD患者的单细胞和炎症性粘膜中,circFNDC3B的表达显著增加.
- 通过转化生长因子-β (TGFβ) 途径,circFNDC3B的下调促进M2巨细胞激活和含有3B (FNDC3B) 表达的纤维素三型域.
- circFNDC3B竞争性地与Hu抗原R (HuR) 结合,防止HuR与FNDC3BmRNA结合,并调节FNDC3B的表达.
- circFNDC3B可以增强单细胞对血管内皮细胞的粘附.
结论:
- 宏特定的circFNDC3B通过circFNDC3B-HuR-FNDC3B-TGFβ轴将宏两极分化为类似M2的表型.
- 这项研究为炎症性肠病 (IBD) 中的单细胞-巨细胞功能提供了新的机制性见解.
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