长非编码RNARMRP通过与PFN1以P53-依赖的方式相互作用来改善多克索鲁比诱导的亡
Juexing Li1, Lei Zhou1, Yuanliang Jiang2
1Department of Cardiology, Jinshan Hospital of Fudan University, Shanghai, 201508, China; Department of Internal Medicine, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Molecular and cellular probes
|October 11, 2023
概括
长非编码RNARMRP在心力衰竭中降低调节,并通过调节PFN1/p53通路来防止多克索鲁比诱导的心脏毒性. 这表明RMRP是心力衰竭的潜在治疗标.
科学领域:
- 心脏病学 心脏病学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 德克索鲁比 (DOX) 化疗可以诱导心脏毒性,导致心力衰竭.
- 长非编码RNARMRP在DOX诱导的心脏毒性和心力衰竭中的作用尚不清楚.
研究的目的:
- 调查RMRP在DOX诱导心脏毒性的作用.
- 阐明涉及心力衰竭RMRP的潜在分子机制.
主要方法:
- 对基因表达数据集的生物信息分析 (GSE124401,GSE149870).
- 在心力衰竭患者和细胞模型的外周血液中验证RMRP表达.
- 使用西方斑点和TUNEL染色来评估亡.
- 双化酶记者测定证实RMRP和PFN1的相互作用.
主要成果:
- 在心力衰竭患者和DOX治疗细胞中,RMRP显著下调.
- 过度表达RMRP减弱的DOX诱导的亡.
- PFN1被确定为RMRP心脏保护作用的直接下游调解者.
- RMRP抑制了PFN1,这反过来又抑制了p53的表达和酸化.
结论:
- RMRP通过PFN1/p53信号轴对DOX诱导的心脏毒性产生心脏保护作用.
- RMRP显示出作为心力衰竭治疗标和生物标记物的潜力.
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