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Publication : Steady-state and regenerative hematopoiesis occurs normally in mice in the absence of GDF11.

First Author  Goldstein JM Year  2019
Journal  Blood Volume  134
Issue  20 Pages  1712-1716
PubMed ID  31530563 Mgi Jnum  J:282097
Mgi Id  MGI:6379161 Doi  10.1182/blood.2019002066
Citation  Goldstein JM, et al. (2019) Steady-state and regenerative hematopoiesis occurs normally in mice in the absence of GDF11. Blood 134(20):1712-1716
abstractText  Tightly regulated production of mature blood cells is essential for health and survival in vertebrates and dependent on discrete populations of blood-forming (hematopoietic) stem and progenitor cells. Prior studies suggested that inhibition of growth differentiation factor 11 (GDF11) through soluble activin receptor type II (ActRII) ligand traps or neutralizing antibodies promotes erythroid precursor cell maturation and red blood cell formation in contexts of homeostasis and anemia. As Gdf11 is expressed by mature hematopoietic cells, and erythroid precursor cell expression of Gdf11 has been implicated in regulating erythropoiesis, we hypothesized that genetic disruption of Gdf11 in blood cells might perturb normal hematopoiesis or recovery from hematopoietic insult. Contrary to these predictions, we found that deletion of Gdf11 in the hematopoietic lineage in mice does not alter erythropoiesis or erythroid precursor cell frequency under normal conditions or during hematopoietic recovery after irradiation and transplantation. In addition, although hematopoietic cell-derived Gdf11 may contribute to the pool of circulating GDF11 protein during adult homeostasis, loss of Gdf11 specifically in the blood system does not impair hematopoietic stem cell function or induce overt pathological consequences. Taken together, these results reveal that hematopoietic cell-derived Gdf11 is largely dispensable for native and transplant-induced blood formation.
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