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Heart regeneration is regulates by key micro RNAs from fish to mammals: what it can learned about the epicardial cells activation during the regeneration in zebrafish

机译:心脏再生是通过来自鱼到哺乳动物的关键微量RNA调节:在斑马鱼的再生过程中,它可以了解的内容性细胞激活

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Zebrafish could be an interesting translational model tounderstand and improve the post-infarction trial andpossible regeneration in mammals. The regenerativecapacity in mammalian heart is maintained partially inneonatal life1 because are still switch-on somephylogenetic-conserved genes; while in adult, it seems toconfined in replacing by a few of cardiomyocytes (CM)and by a large amount of fibroblasts2,3. In contrast, naturalcardiac regeneration appears to be excellent in fish afteran injury. In zebrafish, the cardiac environment created bycardiomyocytes, fibroblasts, and non-muscle cells afterinjury is believed to be critical in facilitating the regenerative response4. The epicardium-derived cells and theconsequent epicardial cells (EPCs) are essential regulatorssince they respond to FGFs in both embryogenesis andregeneration processes. EPCs undergo to number of cellular modifications5,6 that is required to silenced by miRsthat controlled the differentiation of the cells. Thisdownregulation is a necessary event to activate the transition from epithelial to mesenchymal cells, such ascytoskeletal re-arrange and expression of hyaluronanmediated motility receptor, necessaries to move in thedamage site7,8. In the heart several molecules are involvedin the protein synthesis regulation9 where the miRs have aupstream actions. MiR1 and miR133 (a and b) areinvolved in the activation of fibroblasts in producingFGFs10,11, as well as the hypertrophic response of epithelial and muscular cells after injury, to compensate forthe loss-of-contractile tissue in mammals, as well as inzebrafish9,12–14.
机译:斑马鱼可能是一个有趣的翻译模式Tounderstand,改善哺乳动物的梗塞后试验和植物的再生。哺乳动物心脏的再生症被保持部分含肺活动1,因为仍然有关血管发育保守基因;在成年人中,它似乎在替代少数心肌细胞(cm)和大量的成纤维细胞2,3时似乎。相比之下,胰腺再生似乎是鱼苗损伤的优异。在斑马鱼中,据信通过曲线霉细胞,成纤维细胞和非肌肉细胞产生的心脏环境在促进再生反应方面至关重要。表皮衍生的细胞和表皮细胞(EPCS)是必不可少的调节剂,它们在胚胎发生和治疗过程中对FGF进行反应。 EPC经历由MiRSTHAT静音所需的细胞修饰5,6的数量控制细胞的分化。 TheAdownRegulation是激活从上皮细胞的转变的必要事件,这种胱内骨骼重新安排和表达透明化的运动受体,必须在患有TheDamAgeS7,8中移动的必需品。在心脏中,几种分子参与蛋白质合成调节9,其中MIR具有Aupstream作用。 MiR1和miR133(a和b)在产品中的成纤维细胞活化中溶解,以及损伤后上皮和肌肉细胞的肥大响应,以补偿哺乳动物中的收缩丧失组织,以及尿布, 12-14。

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