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Fate determination in mesenchymal stem cells: a perspective from histone-modifying enzymes
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  • 作者:Biao Huang (1)
    Gang Li (2) (3) (4)
    Xiao Hua Jiang (1) (3) (4)

    1. Key Laboratory for Regenerative Medicine
    ; Ministry of Education ; Epithelial Cell Biology Research Centre ; School of Biomedical Sciences ; Lo Kwee-Seong Integrated Biomedical Sciences Building ; Shatin ; New Territories ; Hong Kong ; PR China
    2. Department of Orthopaedics & Traumatology
    ; Li Ka Shing Institute of Health Science ; Prince of Wales Hospital ; 30-32 Ngan Shing Street ; Shatin ; New Territories ; Hong Kong ; PR China
    3. Lui Che Woo Institute of Innovative Medicine
    ; Faculty of Medicine ; The Chinese University of Hong Kong ; Hong Kong ; SAR ; China
    4. School of Biomedical Sciences Core Laboratory
    ; The Chinese University of Hong Kong Shenzhen Research Institute ; Shenzhen ; 518057 ; China
  • 刊名:Stem Cell Research & Therapy
  • 出版年:2015
  • 出版时间:December 2015
  • 年:2015
  • 卷:6
  • 期:1
  • 全文大小:1,017 KB
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  • 刊物主题:Stem Cells; Cell Biology;
  • 出版者:BioMed Central
  • ISSN:1757-6512
文摘
Mesenchymal stem cells (MSCs) hold great promise for therapeutic use in regenerative medicine and tissue engineering. A detailed understanding of the molecular processes governing MSC fate determination will be instrumental in the application of MSCs. Much progress has been made in recent years in defining the epigenetic events that control the differentiation of MSCs into different lineages. A complex network of transcription factors and histone modifiers, in concert with specific transcriptional co-activators and co-repressors, activates or represses MSC differentiation. In this review, we summarize recent progress in determining the effects of histone-modifying enzymes on the multilineage differentiation of MSCs. In addition, we propose that the manipulation of histone signatures associated with lineage-specific differentiation by small molecules has immense potential for the advancement of MSC-based regenerative medicine.

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