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介导诱导性少突胶质细胞祖细胞生成的重编程因子的研究进展

Reprogramming Factors Involved in Generation of Induced Oligodendrocyte Precursor Cells
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摘要 少突胶质细胞(oligodendrocytes, OLs)是中枢神经系统(central nervous system, CNS)中主要的成髓鞘细胞,其功能障碍会引发一系列的神经性疾病,例如:多发性硬化症(multiple sclerosis,MS)和脑白质营养不良。少突胶质细胞祖细胞(oligodendrocyte precursor cells, OPCs)的移植是治疗髓鞘相关疾病的一种潜在方法。在脑损伤后, OPCs可向OLs方向分化并对损伤部位的轴突进行髓鞘化,但是, OPCs在大脑中仅占5%~8%,这种髓鞘修复作用十分有限。通过体外重编程技术生成诱导性少突胶质细胞祖细胞(induced oligodendrocyte precursor cells, iOPCs)的策略可为髓鞘损伤疾病的治疗提供大量的细胞资源。但是该方法仍存在一系列亟待解决的问题,包括i OPCs生成效率较低、体外培养周期较长等。因此,该文从限定性转录因子、miRNA以及小分子物质等方面阐述了iOPCs的生成方法,并分析了iOPCs的现存问题和应用前景,旨在为其在疾病模型构建、药物开发和再生医学等方面的应用提供理论和技术参考。 Oligodendrocytes(OLs) are the major type of myelin-generatingcells in the central nervous system(CNS), dysfunction of them contributes to a variety of neurological diseases, such as multiple sclerosis(MS) and congenital leukodystrophies. Transplantation of oligodendrocyte precursor cells(OPCs) is a promising therapeutic strategy for those demyelinating diseases. After the brain tissue is injured, OPCs will be differentiated into OLs which can remyelinate the axon, but this kind of repairability is very limited because there are only 5% to 8% OPCs in the brain. Reprogramming of mammalian cells into induced OPCs(iOPCs) in vitro is a promising strategy for remyelination, but some problems such as lower productive efficiency and long-time culture for generation of them in vitro need to be solved or improved. Therefore, different induced factors(including defined transcription factors, miRNAs and small molecules), problems and application prospects of iOPCs were reviewed in this paper in order to provide the theoretical and technological guidances for disease modeling, new drug development and regenerative medicine research.
作者 令文慧 王明玉 熊春霞 谢登峰 陈麒宇 褚新月 李云鑫 邱小燕 李跃民 肖雄 Ling Wenhui;Wang Mingyu;Xiong Chunxia;Xie Dengfeng;Chen Qiyu;Chu Xinyue;Li Yunxin;Qiu Xiaoyan;Li Yuemin;Xiao Xiong(College of Animal Science and Technology,Southwest University,Chongqing 400715,China)
出处 《中国细胞生物学学报》 CAS CSCD 2019年第8期1647-1657,共11页 Chinese Journal of Cell Biology
基金 国家自然科学基金(批准号:31572488) 重庆市基础科学与前沿技术研究项目(批准号:cstc2017jcyjAX0477)资助的课题~~
关键词 诱导性少突胶质细胞祖细胞 少突胶质细胞 转录因子 MIRNA 重编程 induced oligodendrocyte precursor cells(iOPCs) oligodendrocytes(OLs) transcription factor miRNA reprogramming
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  • 1Offield MF;Jetton TL;Labosky PA.PDX-1 is required for pancreatic outgrowth and differentiation of the rostral duodenum,1996. 被引量:3
  • 2M. Al-Masri,M. Krishnamurthy,J. Li,G. F. Fellows,H. H. Dong,C. G. Goodyer,R. Wang.Effect of forkhead box O1 (FOXO1) on beta cell development in the human fetal pancreas[J]. Diabetologia . 2010 (4) 被引量:1
  • 3B. M. Lyttle,J. Li,M. Krishnamurthy,F. Fellows,M. B. Wheeler,C. G. Goodyer,R. Wang.Transcription factor expression in the developing human fetal endocrine pancreas[J]. Diabetologia . 2008 (7) 被引量:1
  • 4J. M. Servitja,J. Ferrer.Transcriptional networks controlling pancreatic development and beta cell function[J]. Diabetologia . 2004 (4) 被引量:1
  • 5Hsiang-Po Huang,Ming-Jer Tsai.Transcription factors involved in pancreatic islet development[J]. Journal of Biomedical Science . 2000 (1) 被引量:1
  • 6Jin T.Why diabetes patients are more prone to the develop- ment of colon cancer?. Medical Hypotheses . 2008 被引量:1
  • 7Jin T,Trinh DK,Wang F,Drucker DJ.The caudal homeobox protein cdx-2/3 activates endogenous proglucagon gene expression in InR1-G9 islet cells. Journal of Molecular Endocrinology . 1997 被引量:1
  • 8Wang P,,Liu T,Li Z,Ma X,Jin T.Redundant and synergistic effect of Cdx-2 and Brn-4 on regulating proglucagon gene expression. The Journal of Endocrinology . 2006 被引量:1
  • 9Liu T,Branch DR,Jin T.Pbx1 is a co-factor for Cdx-2 in regu- lating proglucagon gene expression in pancreatic A cells. Molecular and Cellular Endocrinology . 2006 被引量:1
  • 10Xu F,Li H,Jin T.Cell type-specific autoregulation of the Cau- dal-related homeobox gene Cdx-2/3. Journal of Biological Chemistry . 1999 被引量:1

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