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在阻塞性瘤病的纤维化中对lncRNA XIST/miR-124-3p/ITGB1轴的机制研究

ChiTeng Zhang¹, KangNing Wang², Xiang Chen²

¹Department of Urology Surgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang City, Hunan Province, 421001, China.

Experimental cell research

|August 10, 2024

概括

长非编码RNAXIST通过影响miR-124-3p和ITGB1水平来促进纤维化. 降低调节的XIST显示出阻塞性病 (ON) 和纤维化治疗潜力.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
生物化学生化学

背景情况:

纤维化是各种慢性病中常见的病理过程.
阻塞性病 (ON) 是末期病的重要原因,通常导致纤维化.
确定纤维化关键分子机制和治疗点至关重要.

研究的目的:

研究长非编码RNAXIST在与ON相关的纤维化中的作用.
阐明涉及XIST,miR-124-3p和ITGB1.1的潜在分子机制.
探索XIST作为纤维化的潜在治疗标.

主要方法:

在ON患者样本和TGF-β1诱导的HK-2细胞中分析XIST,miR-124-3p和ITGB1表达.
评估细胞活力,增殖,迁移和上皮层-介质细胞过渡 (EMT) 标志物.
通过双 luciferase 记者基因测定和单边尿路阻塞 (UUO) 的 in vivo 小鼠模型验证分子相互作用.

主要成果:

在ON患者和TGF-β1治疗细胞中观察到XIST和ITGB1升高,miR-124-3p降低.
减少XIST或增强miR-124-3p抑制了TGF-β1诱导的HK-2细胞活力,增殖,迁移和EMT.
XIST充当了miR-124-3p的海绵,miR-124-3p对ITGB1进行了负面调节;ITGB1的升高抵消了XIST枯竭效应.
在UUO小鼠中,XIST的下调改善了纤维化.

结论:

在ON中,XIST通过海绵化miR-124-3p并随后增加ITGB1表达来促进纤维化.
向XIST是一个潜在的治疗策略,可以缓解ON的纤维化.

关键词:

根据ITGB1的规定.在 LncRNA XIST 中.阻塞性脏病是一种阻塞性脏病.患有脏纤维化在 miR-124-3p 中使用.

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