Cell cycle analysis of primary grafts revealed decreased frequency of HSCs in G 0, suggesting that lack of Eng impairs reentry of HSCs to quiescence. Transplantation of Eng-deleted whole bone marrow or purified HSCs into lethally irradiated mice results in a profound engraftment defect in tertiary and quaternary recipients. Using conditional deletion of Eng combined with serial transplantation, we show that this TGF-β receptor is critical to maintain the HSC pool. Endoglin (Eng), a type III receptor for the TGF-β superfamily, has been shown to selectively mark long-term HSCs however, its necessity in adult HSCs is unknown due to embryonic lethality. However, the molecular mechanism underlining this function remains obscure. Transforming growth factor β (TGF-β) is well known for its important function in hematopoietic stem cell (HSC) quiescence.
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