TGF-β1 Negatively Regulates the Number and Function of Hematopoietic Stem Cells

• Published in: Stem cell reports 2018-07, Vol.11 (1), p.274-287
• Main Authors: Wang, Xiaofang, Dong, Fang, Zhang, Sen, Yang, Wanzhu, Yu, Wenying, Wang, Zhao, Zhang, Shanshan, Wang, Jinhong, Ma, Shihui, Wu, Peng, Gao, Yun, Dong, Ji, Tang, Fuchou, Cheng, Tao, Ema, Hideo
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Cell Cycle; Cell Differentiation; Cell Division - genetics; Cell Self Renewal; differentiation; G0 phase; Gene Expression Profiling; Gene Expression Regulation; hematopoietic stem cells; Hematopoietic Stem Cells - cytology; Hematopoietic Stem Cells - metabolism; Mice; quiescence; self-renewal; Transforming Growth Factor beta1 - metabolism; transforming growth factor β1
• ISSN: 2213-6711; 2213-6711
• DOI: 10.1016/j.stemcr.2018.05.017

Transforming growth factor β1 (TGF-β1) plays a role in the maintenance of quiescent hematopoietic stem cells (HSCs) in vivo. We asked whether TGF-β1 controls the cell cycle status of HSCs in vitro to enhance the reconstitution activity. To examine the effect of TGF-β1 on the HSC function, we used an in vitro culture system in which single HSCs divide with the retention of their short- and long-term reconstitution ability. Extensive single-cell analyses showed that, regardless of its concentration, TGF-β1 slowed down the cell cycle progression of HSCs but consequently suppressed their self-renewal potential. Cycling HSCs were not able to go back to quiescence with TGF-β1. This study revealed a negative role of TGF-β1 in the regulation of the HSC number and reconstitution activity. [Display omitted] •TGF-β1 slows down the cell cycle progression of HSCs•Cycling HSCs were unable to go back to the G0 state with TGF-β1•TGF-β1 suppresses the self-renewal potential in HSCs•The reduced division rate with TGF-β1 is reversible Dr. Ema and colleagues report in vitro effect of TGF-β1 on single hematopoietic stem cells (HSCs). TGF-β1 slowed down the cell cycle progression of HSCs but consequently suppressed their self-renewal potential. Cycling HSCs were unable to return to quiescence with TGF-β1. This study revealed a negative role of TGF-β1 in the regulation of the HSC number and reconstitution activity.