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长非编码RNA CPR (心肌细胞增殖调节剂) 调节心肌细胞增殖和心脏修复
Murugavel Ponnusamy1, Fang Liu2, Yu-Hui Zhang3
1Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, China (M.P., L.-Y.Z., C.-Y.L., K.-W.L., Y.-H.D., M.W., L.-L.Q., C.S., S.X., Q.W., Yan-Hui Zhang, P.-F.L., K.W.).
Circulation
|March 6, 2019
概括
心肌细胞增殖调节器 (CPR) 抑制了心脏细胞的再生. 抑制心肺复苏促进心肌细胞的增殖和心脏损伤后的修复, 这为心力衰竭提供了新的治疗策略.
科学领域:
- 心血管生物学
- 分子生物学
- 表观遗传学
背景情况:
- 成人心肌细胞失去增殖能力,导致心脏功能障碍和心力衰竭.
- 衰减心肌细胞增殖的分子机制在很大程度上是未知的.
- 长非编码RNAs (lncRNAs) 在心血管疾病中起作用,促使研究其在心肌细胞增殖和修复中的作用.
研究的目的:
- 研究 lncRNAs 在调节心肌细胞增殖和心脏修复中的作用.
- 鉴定和描述一种参与心肌细胞增殖的新型 lncRNA, CPR.
主要方法:
- 生物信息分析以确定潜在的 lncRNA.
- 产生心肺复苏淘汰和心脏特异性心肺复苏过度表达的小鼠.
- 使用隔离心肌细胞进行心肺复苏静音化或过度表达的体外研究.
- 定量PCR,西斑,组织学,心声学,转录组分析,RNA下拉和ChIP测试以阐明心肺复苏功能和机制.
主要成果:
- 成人心脏中的CPR水平高于胎儿心脏.
- 在产后和成人心脏中,心肺复苏静止增加了心肌细胞的增殖,并在心肌损伤后恢复了心脏功能.
- 抑制新生儿心肌细胞的增殖和心脏再生.
- 通过将DNMT3A引入MCM3促进体,抑制心肌细胞增殖并增加其表达.
结论:
- 作为心肌细胞增殖和心脏再生的负调节剂.
- lncRNAs参与调节心肌细胞的增殖和心脏修复.
- 在心脏修复和再生方面,心肺复苏是一种潜在的基于 lncRNA 的治疗点.
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