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外基因组转移的LINC00668通过促进炎症性肠病中的NETs形成,促进血栓形成

Long Zhang¹, Bin Zheng¹, Yang Bai¹

¹Department of Biochemistry and Molecular Biology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education of China, Hebei Medical University, Shijiazhuang, 050017, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|August 17, 2023

概括

炎症性肠病 (IBD) 通过中性粒细胞外细胞陷 (NETs) 促进血栓形成,由外体释放. 用柏柏林 (BBR) 准LINC00668可以治疗IBD相关的血栓.

科学领域:

胃肠病学胃肠病学
血液学血液学血液学
分子生物学分子生物学

背景情况:

炎症性肠病 (IBD) 与较高的血栓形成风险有关.
连接IBD和血栓形成的潜在机制尚未完全理解.

研究的目的:

研究中性粒细胞外细胞陷 (NETs) 在IBD相关血栓形成中的作用.
通过外体细胞识别连接炎症肠上皮细胞 (IECs) 与血栓形成的分子机制.
评估针对这些机制的治疗潜力.

主要方法:

在小鼠中使用硫酸 (DSS) 诱导IBD.
分析NETs的形成及其对血栓形成的贡献.
从IBD小鼠血和炎症IEC中分离和体内测试外体.
外体的RNA测序以识别关键分子.
研究LINC00668在中性粒细胞弹性酶 (NE) 转位和NETs释放中的作用.
评估柏柏林 (BBR) 对LINC00668-NE相互作用和NETs形成的影响.

主要成果:

DSS诱导的IBD小鼠表现出增加的NETs形成,导致血栓形成.
来自IBD小鼠血的外体在体内诱导了动脉和静脉血栓形成.
炎症的IECs分泌出外体,促进中性粒细胞释放NETs.
LINC00668具有高度丰富的炎症IEC衍生的外体,并促进NE核转位,诱导NETs释放和血栓形成.
柏柏林 (BBR) 抑制了LINC00668-NE相互作用,抑制了NE核转位,NETs形成,并产生抗血栓作用.

结论:

一个新的机制通过外体介导NETs的形成将IBD和血栓形成.
通过促进NE驱动的NET释放,LINC00668在IBD中促进血栓形成方面发挥着关键作用.
针对LINC00668代表了IBD相关血栓形成的潜在治疗策略.

关键词:

我们的 LINC0066868 联系方式贝贝林 (Berberine) 是一种葡萄酒.外基因组是外基因组的组成部分.炎症性肠道疾病炎症性肠道疾病中性粒细胞弹性酶.中性粒细胞外细胞陷血栓形成的原因是因为血栓.

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