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| 1 | Micromanaging cardiac regeneration:Targeted delivery of micro RNAs for cardiac repair and regeneration显示文摘The loss of cardiomyocytes during injury and disease can result in heart failure and sudden death, while the adult heart has a limited capacity for endogenous regeneration and repair. Current stem cell-based regenerative medicine approaches modestly improve cardiomyocyte survival, but offer neglectable cardiomyogenesis. This has prompted the need for methodological developments that crease de novo cardiomyocytes. Current insights in cardiac development on the processes and regulatory mechanisms in embryonic cardiomyocyte differentiation provide a basis to therapeutically induce these pathways to generate new cardiomyocytes. Here, we discuss the current knowledge on embryonic cardiomyocyte differentiation and the implementation of this knowledge in state-ofthe-art protocols to the direct reprogramming of cardiac fibroblasts into de novo cardiomyocytes in vitro and in vivo with an emphasis on micro RNA-mediated reprogramming. Additionally, we discuss current advances on state-of-theart targeted drug delivery systems that can be employed to deliver these micro RNAs to the damaged cardiac tissue. Together, the advances in our understanding of cardiac development, recent advances in micro RNAbased therapeutics, and innovative drug delivery systems, highlight exciting opportunities for effective therapies for myocardial infarction and heart failure. | Jan AAM Kamps Guido Krenning | 2016 | World Journal of Cardiology2016，8，2： | 6 |
| 2 | Popdc2表达下调通过Akt磷酸化促进新生大鼠心肌细胞增殖显示文摘目的 :探讨Popdc2对新生大鼠心肌细胞增殖作用及其机制。方法 :分离出生后第0、7、14天大鼠心脏组织,荧光定量逆转录-聚合酶链反应(q RT-PCR)检测心脏组织中Popdc2 m RNA表达情况。分离出生后0~2 d SD大鼠原代心肌细胞和成纤维细胞,q RT-PCR检测Popdc家族m RNA在心肌细胞表达情况、Popdc2 m RNA在心肌细胞和成纤维细胞表达情况;大鼠原代心肌细胞分别转染阴性对照小干扰RNA(NC组)和Popdc2特异性小干扰RNA(si-Popdc2组),Ed U实验、Ki67染色检测心肌细胞增殖,免疫荧光检测心肌细胞特异性蛋白辅肌动蛋白(actinin)和心肌钙蛋白2(TNNT2)表达,q RT-PCR检测转染小干扰RNA后心肌细胞Popdc2及转录因子TBX20、TBX5 m RNA表达、增殖抗原蛋白Ki67 m RNA表达情况,Western blot检测总Akt及磷酸化Akt蛋白表达水平。结果:1 Popdc家族中Popdc2 m RNA在心肌细胞表达最高(P均<0.01),且随着出生后天数增加Popdc2表达逐渐升高(P均<0.01),Popdc2 m RNA在心肌细胞表达高于成纤维细胞(P<0.05);2与对照组相比,沉默Popdc2可促进原代心肌细胞DNA合成(P<0.05),并增加Ki67阳性心肌细胞数量(P<0.05);3q RT-PCR显示沉默Popdc2可上调转录因子TBX20(P<0.01)、TBX5(P<0.05)的m RNA表达,沉默Popdc2促进Ki67的m RNA表达(P<0.05),Western blot结果显示沉默Popdc2可促进Akt蛋白磷酸化,Akt308(P<0.05),Akt473(P<0.001)。结论 :Popdc2表达下调可能通过调节转录因子表达及Akt蛋白磷酸化促进新生大鼠心肌细胞增殖,Popdc2有可能成为心肌损伤后修复和再生治疗靶点。 | 魏飞宇 吕丽 马方方 周蕾 | 2015 | 南京医科大学学报(自然科学版)2015，35，7： | 2 |
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