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一种新的lncRNA ABCE1-5通过准KRT14来调节肺纤维化

Shuwei Gao^1,2,3,4, Yanqiu Wei^1,2,3,4, Chen Li^1,2,3,4

¹National Center for Respiratory Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, People's Republic of China.

American journal of physiology. Cell physiology

|March 20, 2025

概括

一种新的长非编码RNA,ABCE1-5,被发现在异常性肺纤维化 (IPF) 中降低. 较低的ABCE1-5水平通过激活素14和mTOR/AKT信号来促进纤维化,这表明ABCE1-5是IPF的潜在治疗标.

科学领域:

分子生物学分子生物学
肺部医学肺部医学
在RNA生物学,RNA生物学.

背景情况:

异形性肺纤维化 (IPF) 是一种渐进的肺病,死亡率高,病因不明.
长非编码RNAs (lncRNAs) 越来越被认为是纤维性疾病的调节者,但它们在IPF中的特定作用需要进一步研究.
识别新型分子参与者对于理解IPF进展和开发向疗法至关重要.

研究的目的:

识别和描述参与IPF病变发生的新型lncRNAs.
阐明IncABCE1-5调节肺纤维化的分子机制.
在IPF的临床前模型中评估IncABCE1-5的治疗潜力.

主要方法:

ncRNA微阵列分析和qRT-PCR用于识别IPF肺组织中差异表达的lncRNA.
在体外 (细胞系) 和体内 (小鼠模型) 的功能损失和功能增益实验为lncABCE1-5.5.
拉下RNA质谱和RNA免疫沉试验,以确定lncABCE1-5.5的直接结合标.
西部涂抹以评估蛋白质表达和酸化水平 (mTOR,Akt).

主要成果:

一种新的lncRNA,ABCE1-5,在IPF肺样本中显著下调.
沉默lncABCE1-5促进了细胞迁移,细胞亡和细胞外基质沉积,而其过度表达减弱了TGF-β诱导的纤维生成.
lncABCE1-5直接与素14 (krt14) 结合,抑制其表达,并随后减少mTOR/AKT信号激活.
在白血素诱导的肺纤维化小鼠模型中,IncABCE1-5的过度表达减少了纤维化和减弱的mTOR/AKT酸化.

结论:

这项研究确定了IncABCE1-5作为IPF中的新型抗纤维素IncRNA.
低调 lncABCE1-5 通过激活 krt14-mTOR/AKT 信号轴,促进肺纤维化.
ABCE1-5-krt14-mTOR轴代表了IPF治疗的潜在治疗目标.

关键词:

在ABCE1-5中.在KRT-14中,长非编码RNA的编码在mTOROR中使用mTOR.肺部纤维化肺部纤维化

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