Gdf15 regulates murine stress erythroid progenitor proliferation and the development of the stress erythropoiesis niche.

ABSTRACT: Anemic stress induces the proliferation of stress erythroid progenitors in the murine spleen that subsequently differentiate to generate erythrocytes to maintain homeostasis. This process relies on the interaction between stress erythroid progenitors and the signals generated in the splenic erythroid niche. In this study, we demonstrate that although growth-differentiation factor 15 (Gdf15) is not required for steady-state erythropoiesis, it plays an essential role in stress erythropoiesis. Gdf15 acts at 2 levels. In the splenic niche, Gdf15^-/- mice exhibit defects in the monocyte-derived expansion of the splenic niche, resulting in impaired proliferation of stress erythroid progenitors and production of stress burst forming unit-erythroid cells. Furthermore, Gdf15 signaling mai

SUBMITTER: Hao S 

PROVIDER: S-EPMC6650738 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature