The receptor tyrosine kinase c-kit and its ligand Stem Cell Factor (SCF, also c-kit ligand, Steel factor or mast cell growth factor) are essential for hematopoietic development since mice lacking functional c-kit (White Spotting or W mutants) or SCF (Steel or Sl mutants) die of a severe anemia in utero [14], [20].
Ema, M. et al. Combinatorial effects of Flk1 and Tal1 on vascular and hematopoietic development in the mouse.
For instance, Pimanda et al. described that Gata2, Fli1, and Scl/Tal1 formed a regulatory circuit to regulate early hematopoietic development in the mouse model [ 1].
Importantly, knockdown of miR-146a in mouse hematopoietic stem cells resulted in the development of some hematological abnormalities, such as neutropenia and megakaryocytic dysplasia, typically observed in myelodysplastic syndromes.
Reciprocal transplantation of CD45.2+ BM cells from diseased RBP-JK5 mice into CD45.1+ wild-type recipient mice (reconstitution efficiency >80%) led to normal hematopoietic development as expected (Figure S6B).
Since CYLD has been implicated in T cell development [7], [11] the hematopoietic development in M-CyldΔ9 mice was evaluated.
Undifferentiated hESCs were harvested and plated on a monolayer of OP9 mouse bone marrow stromal cells capable of promoting hematopoietic development.
As the fetal liver represents the major organ of hematopoietic development during the fetal period in mice as well as in humans, these findings indicate a disturbed hematopoiesis in fetal Ts1Cje mice.
Katsoulidis et al. [14] have also implicated Slfn2 in hematopoietic development; they reported that Slfn2 knockdown promoted mouse hemopoietic colony formation and impaired the growth suppressive actions of IFN-α.
MiR-150 expresses in mature B and T cells derived from mouse hematopoietic stem cells, and is able to block early B cell development when expressed prematurely [ 12].
