miR-1224通过靶向Dlx1 mRNA的3'-UTR调控哺乳动物大脑皮层发育。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Chenglong Liu, Liyu Zhou, Qingbai Liu, Li Ni, Jianping Yang
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引用次数: 0

摘要

神经前体细胞(Neural precursor cells, npc)是一类具有自我更新和多向分化潜能的细胞。microrna是中枢神经系统(CNS)神经发生所必需的。最近的报道表明,miR-1224在人类中枢神经系统疾病中很重要。然而,其在脑发育神经发生中的作用尚不清楚。目前的研究表明,在发展新皮层的过程中,这是必不可少的。结果表明,miR-1224促进更多的npc向神经元和少突胶质细胞分化,同时抑制星形胶质细胞的分化。相反,抑制miR-1224可增强NPCs的自我更新能力和凋亡。通过在体内进行子宫内电穿孔来检测miR-1224在发育中的新皮层中的作用。观察到耗竭阻碍了上层Cux1+神经元的生成,同时使放射状胶质细胞转化为IPCs。然而,miR-1224促进了鼻咽癌在心室区的增殖。此外,miR-1224通过直接靶向mRNA 3'-UTR区域,负向调节nlx1在npc中的表达。这些发现表明miR-1224在皮层发育过程中是一个重要的NPC神经发生调节剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-1224 Controls Mammal Cerebral Cortex Development by Targeting the 3’-UTR of the Dlx1 mRNA

Neural precursor cells (NPCs) are a group of cells with self-renewal and multi-differentiation potential. MicroRNAs are required for neurogenesis in the central nervous system (CNS). Recent reports suggest that miR-1224 is important in human CNS diseases. However, its function in neurogenesis of brain development is unclear. The current study demonstrated the essential while developing the neocortex. The results showed that miR-1224 facilitated more NPCs to differentiate into neurons and oligodendrocytes while suppressing astrocyte differentiation. Conversely, inhibition of miR-1224 enhances the self-renewal ability and apoptosis of NPCs. The role of miR-1224 in the developing neocortex was examined by performing in-utero electroporation in vivo. It was observed that depletion impeded upper-layer Cux1+ neuronal generation while transforming radial glial cells into IPCs. However, miR-1224 promoted NPC proliferation in the ventricular zone. Moreover, miR-1224 negatively regulated the expression of Dlx1 in NPCs by directly targeting the mRNA 3’-UTR region. These findings indicated that miR-1224 is a crucial NPC neurogenesis regulator during cortical development.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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