EDAG promotes the expansion and survival of human CD34+ cells.
Ke ZhaoWei-Wei ZhengXiao-Ming DongRong-Hua YinRui GaoXiu LiJin-Fang LiuYi-Qun ZhanMiao YuHui ChenChang-Hui GeHong-Mei NingXiao-Ming YangChang-Yan LiPublished in: PloS one (2018)
EDAG is multifunctional transcriptional regulator primarily expressed in the linloc-kit+Sca-1+ hematopoietic stem cells (HSC) and CD34+ progenitor cells. Previous studies indicate that EDAG is required for maintaining hematopoietic lineage commitment balance. Here using ex vivo culture and HSC transplantation models, we report that EDAG enhances the proliferative potential of human cord blood CD34+ cells, increases survival, prevents cell apoptosis and promotes their repopulating capacity. Moreover, EDAG overexpression induces rapid entry of CD34+ cells into the cell cycle. Gene expression profile analysis indicate that EDAG knockdown leads to down-regulation of various positive cell cycle regulators including cyclin A, B, D, and E. Together these data provides novel insights into EDAG in regulation of expansion and survival of human hematopoietic stem/progenitor cells.
Keyphrases
- cell cycle
- cell proliferation
- induced apoptosis
- endothelial cells
- cell cycle arrest
- stem cells
- cord blood
- transcription factor
- gene expression
- bone marrow
- cell death
- signaling pathway
- endoplasmic reticulum stress
- pluripotent stem cells
- nk cells
- pi k akt
- risk assessment
- free survival
- mouse model
- quantum dots
- big data
- single cell
- cancer therapy
- heat stress
- human health
- metal organic framework