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

Siyang Hao, Jie Xiang, Dai Chen Wu, James W. Fraser, Baiye Ruan, Jingwei Cai, Andrew David Patterson, Zhi-chun Lai, Robert Paulson

Research output: Contribution to journalArticle

1 Citation (Scopus)

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, Gdf152/2 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 maintains the hypoxia-dependent expression of the niche signal, Bmp4, whereas in stress erythroid progenitors, Gdf15 signaling regulates the expression of metabolic enzymes, which contribute to the rapid proliferation of stress erythroid progenitors. Thus, Gdf15 functions as a comprehensive regulator that coordinates the stress erythroid microenvironment with the metabolic status of progenitors to promote stress erythropoiesis.

Original languageEnglish (US)
Pages (from-to)2205-2217
Number of pages13
JournalBlood Advances
Volume3
Issue number14
DOIs
StatePublished - Jul 23 2019

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Growth Differentiation Factor 15
Erythropoiesis
Erythroid Cells
Monocytes
Homeostasis
Spleen
Erythrocytes
Enzymes

All Science Journal Classification (ASJC) codes

  • Hematology

Cite this

Hao, Siyang ; Xiang, Jie ; Wu, Dai Chen ; Fraser, James W. ; Ruan, Baiye ; Cai, Jingwei ; Patterson, Andrew David ; Lai, Zhi-chun ; Paulson, Robert. / Gdf15 regulates murine stress erythroid progenitor proliferation and the development of the stress erythropoiesis niche. In: Blood Advances. 2019 ; Vol. 3, No. 14. pp. 2205-2217.
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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, Gdf152/2 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 maintains the hypoxia-dependent expression of the niche signal, Bmp4, whereas in stress erythroid progenitors, Gdf15 signaling regulates the expression of metabolic enzymes, which contribute to the rapid proliferation of stress erythroid progenitors. Thus, Gdf15 functions as a comprehensive regulator that coordinates the stress erythroid microenvironment with the metabolic status of progenitors to promote stress erythropoiesis.",
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Gdf15 regulates murine stress erythroid progenitor proliferation and the development of the stress erythropoiesis niche. / Hao, Siyang; Xiang, Jie; Wu, Dai Chen; Fraser, James W.; Ruan, Baiye; Cai, Jingwei; Patterson, Andrew David; Lai, Zhi-chun; Paulson, Robert.

In: Blood Advances, Vol. 3, No. 14, 23.07.2019, p. 2205-2217.

Research output: Contribution to journalArticle

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AU - Cai, Jingwei

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AU - Paulson, Robert

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