A new mechanism for the steady-state regulation of hematopoietic stem cells has been revealed

The Wang Jinyong Group of the Guangzhou Institute of Biomedicine and Health of the Chinese Academy of Sciences and the National Key Laboratory of Experimental Hematology of the Chinese Academy of Medical Sciences, Cheng Hui/Cheng Tao, collaborated to make a new breakthrough in the field of steady-state regulation of hematopoietic stem cells. The study was published online in Hematology. It is reported that Wang Tongjie, Xia Chengxiang as the article's co-first author, Wang Jinyong and Cheng Hui as the co-communications author.
hematopoietic stem cells (HSCs) have the ability to renew themselves and differentiate into a variety of blood cells. Physiologically, HSC is mostly dormant, with only a small number of cells proliferating to maintain hematostation. In some stress states (e.g. excessive blood loss, radiation damage, chemotherapy, etc.), HSC can quickly activate from the sleep state for blood production, when the body returns to normal state, HSC will re-enter the sleep state. This kind of precise steady state maintenance is regulated by complex mechanism, so far, the balance control mechanism between HSC sleep state and active state is not clear.
study found that
expression levels of the gene in HSC were significantly higher than those of hematocytes. To study
role of the disease in HSC, the
model of a mouse that was subject to a conditional knock-out. It was found that the missing HSC of
entered the cell cycle more in physiological steady state, and the competitive transplantation experiment showed that Nupr1-/- HSC had transplant competitive advantage in the body, and the in vitro amplification experiment also showed that Nupr1-/- HSC had stronger proliferation ability.
further transcription group sequencing results reveal that the
The p53 signal path of the HSC is significantly reduced, followed by a correction of the p53 expression level in the
HSC, which reduces its competitive advantage, indicating that the
's steady state adjustment to the HSC is achieved through the p53 signal path. This study is of great theoretical significance for seeking means to intervene in HSC amplification, dry maintenance and promoting implantation.
The study found that transcription factor
regulates the conversion of HSC sleep state and activation state through p53 signal path, knocks out the HSC of
more in the proliferation period and has a stronger transplant competitive advantage, this discovery reveals the new mechanism of HSC steady state regulation. (Source: China Science Journal Zhu Hanbin Huang Boquan)
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