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Article: Metabolic regulation of stress erythropoiesis, outstanding questions, and possible paradigms.

Ruan, Baiye / Paulson, Robert F

2023 Volume 13, Page(s) 1063294

Abstract: Steady state erythropoiesis produces new erythrocytes at a constant rate to replace the senescent cells that are removed by macrophages in the liver and spleen. However, infection and tissue damage disrupt the production of erythrocytes by steady state ... ...

Abstract	Steady state erythropoiesis produces new erythrocytes at a constant rate to replace the senescent cells that are removed by macrophages in the liver and spleen. However, infection and tissue damage disrupt the production of erythrocytes by steady state erythropoiesis. During these times, stress erythropoiesis is induced to compensate for the loss of erythroid output. The strategy of stress erythropoiesis is different than steady state erythropoiesis. Stress erythropoiesis generates a wave of new erythrocytes to maintain homeostasis until steady state conditions are resumed. Stress erythropoiesis relies on the rapid proliferation of immature progenitor cells that do not differentiate until the increase in serum Erythropoietin (Epo) promotes the transition to committed progenitors that enables their synchronous differentiation. Emerging evidence has revealed a central role for cell metabolism in regulating the proliferation and differentiation of stress erythroid progenitors. During the initial expansion stage, the immature progenitors are supported by extensive metabolic changes which are designed to direct the use of glucose and glutamine to increase the biosynthesis of macromolecules necessary for cell growth and division. At the same time, these metabolic changes act to suppress the expression of genes involved in erythroid differentiation. In the subsequent transition stage, changes in niche signals alter progenitor metabolism which in turn removes the inhibition of erythroid differentiation generating a bolus of new erythrocytes to alleviate anemia. This review summarizes what is known about the metabolic regulation of stress erythropoiesis and discusses potential mechanisms for metabolic regulation of proliferation and differentiation.
Language	English
Publishing date	2023-01-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.1063294
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Article ; Online: Epo receptor marks the spot.

Paulson, Robert F

Blood

2019 Volume 134, Issue 5, Page(s) 413–414

MeSH term(s)	Erythroblasts ; Gene Expression Profiling ; Macrophages ; Receptors, Erythropoietin/genetics
Chemical Substances	Receptors, Erythropoietin
Language	English
Publishing date	2019-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2019001581
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Article ; Online: Intra-Peritoneal Transplantation for Generating Acute Myeloid Leukemia in Mice.

Qian, Fenghua / Arner, Brooke E / Nettleford, Shaneice K / Paulson, Robert F / Prabhu, K Sandeep

Journal of visualized experiments : JoVE

2023 , Issue 191

Abstract: There is an unmet need for novel therapies to treat acute myeloid leukemia (AML) and the associated relapse that involves persistent leukemia stem cells (LSCs). An experimental AML rodent model to test therapies based on successfully transplanting these ... ...

Abstract	There is an unmet need for novel therapies to treat acute myeloid leukemia (AML) and the associated relapse that involves persistent leukemia stem cells (LSCs). An experimental AML rodent model to test therapies based on successfully transplanting these cells via retro-orbital injections in recipient mice is fraught with challenges. The aim of this study was to develop an easy, reliable, and consistent method to generate a robust murine model of AML using an intra-peritoneal route. In the present protocol, bone marrow cells were transduced with a retrovirus expressing human MLL-AF9 fusion oncoprotein. The efficiency of lineage negative (Lin
MeSH term(s)	Mice ; Animals ; Humans ; Leukemia, Myeloid, Acute/therapy ; Leukemia, Myeloid, Acute/pathology ; Bone Marrow/pathology ; Bone Marrow Cells
Language	English
Publishing date	2023-01-06
Publishing country	United States
Document type	Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/64834
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Article ; Online: Stress erythropoiesis: definitions and models for its study.

Paulson, Robert F / Hariharan, Sneha / Little, Jane A

Experimental hematology

2020 Volume 89, Page(s) 43–54.e2

Abstract: Steady-state erythropoiesis generates new erythrocytes at a constant rate, and it has enormous productive capacity. This production is balanced by the removal of senescent erythrocytes by macrophages in the spleen and liver. Erythroid homeostasis is ... ...

Abstract	Steady-state erythropoiesis generates new erythrocytes at a constant rate, and it has enormous productive capacity. This production is balanced by the removal of senescent erythrocytes by macrophages in the spleen and liver. Erythroid homeostasis is highly regulated to maintain sufficient erythrocytes for efficient oxygen delivery to the tissues, while avoiding viscosity problems associated with overproduction. However, there are times when this constant production of erythrocytes is inhibited or is inadequate; at these times, erythroid output is increased to compensate for the loss of production. In some cases, increased steady-state erythropoiesis can offset the loss of erythrocytes but, in response to inflammation caused by infection or tissue damage, steady-state erythropoiesis is inhibited. To maintain homeostasis under these conditions, an alternative stress erythropoiesis pathway is activated. Emerging data suggest that the bone morphogenetic protein 4 (BMP4)-dependent stress erythropoiesis pathway is integrated into the inflammatory response and generates a bolus of new erythrocytes that maintain homeostasis until steady-state erythropoiesis can resume. In this perspective, we define the mechanisms that generate new erythrocytes when steady-state erythropoiesis is impaired and discuss experimental models to study human stress erythropoiesis.
MeSH term(s)	Animals ; Bone Morphogenetic Protein 4/genetics ; Bone Morphogenetic Protein 4/immunology ; Cellular Senescence/immunology ; Cytokines/genetics ; Cytokines/immunology ; Erythrocytes/cytology ; Erythrocytes/immunology ; Erythroid Precursor Cells/cytology ; Erythroid Precursor Cells/immunology ; Erythropoiesis/genetics ; Erythropoiesis/immunology ; Gene Expression Regulation ; Humans ; Inflammation ; Liver/cytology ; Liver/immunology ; Macrophages/cytology ; Macrophages/immunology ; Mice ; Models, Biological ; Phagocytosis ; Spleen/cytology ; Spleen/immunology ; Stress, Physiological/genetics ; Stress, Physiological/immunology
Chemical Substances	BMP4 protein, human ; Bone Morphogenetic Protein 4 ; Cytokines
Language	English
Publishing date	2020-08-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2020.07.011
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Article ; Online: Targeting a new regulator of erythropoiesis to alleviate anemia.

Paulson, Robert F

Nature medicine

2012 Volume 20, Issue 4, Page(s) 334–335

MeSH term(s)	Activin Receptors, Type II/metabolism ; Anemia/blood ; Anemia/drug therapy ; Animals ; Autocrine Communication/physiology ; Bone Morphogenetic Proteins/antagonists & inhibitors ; Bone Morphogenetic Proteins/metabolism ; Cell Differentiation ; Disease Models, Animal ; Erythroblasts/metabolism ; Erythropoiesis/drug effects ; Fas Ligand Protein ; Gene Amplification/physiology ; Growth Differentiation Factors/antagonists & inhibitors ; Growth Differentiation Factors/metabolism ; Haplorhini ; Hematinics/pharmacology ; Ligands ; Mice ; Oxidative Stress/physiology ; Reactive Oxygen Species ; Recombinant Fusion Proteins/pharmacology ; beta-Thalassemia/blood ; beta-Thalassemia/drug therapy ; fas Receptor
Chemical Substances	ACE-011 ; Bone Morphogenetic Proteins ; Fas Ligand Protein ; GDF11 protein, human ; Gdf11 protein, mouse ; Growth Differentiation Factors ; Hematinics ; Ligands ; Reactive Oxygen Species ; Recombinant Fusion Proteins ; fas Receptor ; Activin Receptors, Type II (EC 2.7.11.30) ; activin receptor type II-A (EC 2.7.11.30)
Language	English
Publishing date	2012-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.3524
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Article ; Online: Stress Erythropoiesis is a Key Inflammatory Response.

Paulson, Robert F / Ruan, Baiye / Hao, Siyang / Chen, Yuanting

Cells

2020 Volume 9, Issue 3

Abstract: Bone marrow medullary erythropoiesis is primarily homeostatic. It produces new erythrocytes at a constant rate, which is balanced by the turnover of senescent erythrocytes by macrophages in the spleen. Despite the enormous capacity of the bone marrow to ... ...

Abstract	Bone marrow medullary erythropoiesis is primarily homeostatic. It produces new erythrocytes at a constant rate, which is balanced by the turnover of senescent erythrocytes by macrophages in the spleen. Despite the enormous capacity of the bone marrow to produce erythrocytes, there are times when it is unable to keep pace with erythroid demand. At these times stress erythropoiesis predominates. Stress erythropoiesis generates a large bolus of new erythrocytes to maintain homeostasis until steady state erythropoiesis can resume. In this review, we outline the mechanistic differences between stress erythropoiesis and steady state erythropoiesis and show that their responses to inflammation are complementary. We propose a new hypothesis that stress erythropoiesis is induced by inflammation and plays a key role in maintaining erythroid homeostasis during inflammatory responses.
MeSH term(s)	Animals ; Erythropoiesis/immunology ; Humans ; Inflammation/immunology ; Mice ; Stress, Physiological/immunology
Language	English
Publishing date	2020-03-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9030634
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Article ; Online: Development of SKI-349, a dual-targeted inhibitor of sphingosine kinase and microtubule polymerization.

Hengst, Jeremy A / Hegde, Shailaja / Paulson, Robert F / Yun, Jong K

Bioorganic & medicinal chemistry letters

2020 Volume 30, Issue 20, Page(s) 127453

Abstract: Our sphingosine kinase inhibitor (SKI) optimization studies originated with the optimization of the SKI-I chemotype by replacement of the substituted benzyl rings with substituted phenyl rings giving rise to the discovery of SKI-178. We have recently ... ...

Abstract	Our sphingosine kinase inhibitor (SKI) optimization studies originated with the optimization of the SKI-I chemotype by replacement of the substituted benzyl rings with substituted phenyl rings giving rise to the discovery of SKI-178. We have recently reported that SKI-178 is a dual-targeted inhibitor of both sphingosine kinase isoforms (SphK1/2) and a microtubule disrupting agent (MDA). In mechanism-of-action studies, we have shown that these two separate actions synergize to induce cancer cell death in acute myeloid leukemia (AML) cell and animal models. Owning to the effectiveness of SKI-178, we sought to further refine the chemotype while maintaining "on-target" SKI and MDA activities. Herein, we modified the "linker region" between the substituted phenyl rings of SKI-178 through a structure guided approach. These studies have yielded the discovery of an SKI-178 congener, SKI-349, with log-fold enhancements in both SphK inhibition and cytotoxic potency. Importantly, SKI-349 also demonstrates log-fold improvements in therapeutic efficacy in a retro-viral transduction model of MLL-AF9 AML as compared to previous studies with SKI-178. Together, our results strengthen the hypothesis that simultaneous targeting of the sphingosine kinases (SphK1/2) and the induction of mitotic spindle assembly checkpoint arrest, via microtubule disruption, might be an effective therapeutic strategy for hematological malignancies including AML.
MeSH term(s)	Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Drug Development ; Drug Screening Assays, Antitumor ; Enzyme Inhibitors/chemical synthesis ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Humans ; Microtubules/drug effects ; Microtubules/metabolism ; Molecular Structure ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Polymerization/drug effects ; Structure-Activity Relationship
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; sphingosine kinase (EC 2.7.1.-) ; sphingosine kinase 2, human (EC 2.7.1.91)
Language	English
Publishing date	2020-07-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2020.127453
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Article ; Online: Erythropoiesis lagging? pIgA1 steps in to assist Epo.

Paulson, Robert F

Nature medicine

2011 Volume 17, Issue 11, Page(s) 1346–1348

MeSH term(s)	Anemia/physiopathology ; Animals ; Cell Proliferation ; Erythroblasts/physiology ; Erythropoiesis/physiology ; Humans ; Immunoglobulin A/metabolism
Chemical Substances	Immunoglobulin A
Language	English
Publishing date	2011-11-07
Publishing country	United States
Document type	News ; Comment
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.2501
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Article ; Online: Monocyte-derived macrophages expand the murine stress erythropoietic niche during the recovery from anemia.

Liao, Chang / Prabhu, K Sandeep / Paulson, Robert F

Blood

2018 Volume 132, Issue 24, Page(s) 2580–2593

Abstract: Anemic stress induces a physiological response that includes the rapid production of new erythrocytes. This process is referred to as stress erythropoiesis. It is best understood in the mouse where it is extramedullary and utilizes signals and progenitor ...

Abstract	Anemic stress induces a physiological response that includes the rapid production of new erythrocytes. This process is referred to as stress erythropoiesis. It is best understood in the mouse where it is extramedullary and utilizes signals and progenitor cells that are distinct from bone marrow steady-state erythropoiesis. The development of stress erythroid progenitors occurs in close association with the splenic stress erythropoiesis niche. In particular, macrophages in the niche are required for proper stress erythropoiesis. Here we show that the expansion of the niche occurs in concert with the proliferation and differentiation of stress erythroid progenitors. Using lineage tracing analysis in 2 models of anemic stress, we show that the expansion of the splenic niche is due to the recruitment of monocytes into the spleen, which develop into macrophages that form erythroblastic islands. The influx in monocytes into the spleen depends in part on Ccr2-dependent signaling mediated by Ccl2 and other ligands expressed by spleen resident red pulp macrophages. Overall, these data demonstrate the dynamic nature of the spleen niche, which rapidly expands in concert with the stress erythroid progenitors to coordinate the production of new erythrocytes in response to anemic stress.
MeSH term(s)	Anemia/genetics ; Anemia/metabolism ; Anemia/pathology ; Animals ; Chemokine CCL2/genetics ; Disease Models, Animal ; Erythropoiesis ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Knockout ; Monocytes/metabolism ; Monocytes/pathology ; Signal Transduction ; Stress, Physiological
Chemical Substances	Ccl2 protein, mouse ; Chemokine CCL2
Language	English
Publishing date	2018-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2018-06-856831
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Article ; Online: Interleukin-4 treatment reduces leukemia burden in acute myeloid leukemia.

Qian, Fenghua / Arner, Brooke E / Kelly, Kathleen M / Annageldiyev, Charyguly / Sharma, Arati / Claxton, David F / Paulson, Robert F / Prabhu, K Sandeep

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2022 Volume 36, Issue 5, Page(s) e22328

Abstract: Interleukin-4 (IL-4) is a signature cytokine pivotal in Type 2 helper T cell (Th2) immune response, particularly in allergy and hypersensitivity. Interestingly, IL-4 increases endogenous levels of prostaglandin ... ...

Abstract	Interleukin-4 (IL-4) is a signature cytokine pivotal in Type 2 helper T cell (Th2) immune response, particularly in allergy and hypersensitivity. Interestingly, IL-4 increases endogenous levels of prostaglandin D
MeSH term(s)	Animals ; Cytokines ; Humans ; Interleukin-4/pharmacology ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/metabolism ; Mice ; PPAR gamma/metabolism ; Prostaglandin D2/metabolism
Chemical Substances	Cytokines ; PPAR gamma ; Interleukin-4 (207137-56-2) ; Prostaglandin D2 (RXY07S6CZ2)
Language	English
Publishing date	2022-04-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202200251R
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