长非编码RNAANRIL通过miR-191-5p/SATB1轴调节性结肠炎中的炎症因子表达
Ke-Qi Yu1, Chuan-Fei Li1, Lu Ye1
1Department of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Yuzhong, Chongqing, 400010, China.
Inflammation
|November 20, 2023
概括
长非编码RNAANRIL通过通过miR-191-5p/SATB1通路抑制IL-6和TNF-α来抑制性结肠炎 (UC) 的进展. 较低的ANRIL水平与UC严重程度相关.
科学领域:
- 分子生物学分子生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 性结肠炎 (UC) 是一种具有显著发病率的炎症性肠病.
- 导致UC病变的精确分子机制尚不完全理解.
- 在UC患者中观察到长非编码RNA (lncRNA) ANRIL的减少表达,但其功能作用尚不清楚.
研究的目的:
- 阐明 lncRNA ANRIL 影响性结肠炎的机制.
- 研究ANRIL/miR-191-5p/SATB1轴在调节UC中的关键炎性细胞因子中的作用.
主要方法:
- 在UC患者组织中分析ANRIL,IL-6和TNF-α的表达.
- 使用LPS治疗的FHC进行体外研究,以评估ANRIL对细胞因子产生的影响.
- 双 luciferase 记者测定证实ANRIL,miR-191-5p和SATB1.1.p之间的直接相互作用.
- 使用DSS诱导的大肠炎小鼠模型进行体内研究,以评估ANRIL对疾病进展的影响.
主要成果:
- 在UC患者中,ANRIL的表达显著下降,与疾病严重程度相关.
- 降低ANRIL的调节导致IL-6和TNF-α表达在体外增加.
- ANRIL直接向并抑制miR-191-5p,从而导致SATB1的上调.
- 过度表达miR-191-5p可以逆转ANRIL对IL-6和TNF-α的抑制作用.
- 在小鼠中,ANRIL缺乏症加剧了DSS诱导的大肠炎.
结论:
- 通过调节miR-191-5p/SATB1轴,ANRIL作为UC炎症的关键抑制剂.
- 这项研究确定了一种参与UC进展的新型分子途径.
- ANRIL/miR-191-5p/SATB1轴代表了性结肠炎的潜在治疗.
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