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Article: Helminth infection impacts hematopoiesis.

Wijshake, Tobias / Wang, Jipeng / Rose, Joseph / Marlar-Pavey, Madeleine / Collins, James J / Agathocleous, Michalis

bioRxiv : the preprint server for biology

2023

Abstract: Helminth infections are common in animals. However, the impact of a helminth infection on the function of hematopoietic stem cells (HSCs) and other hematopoietic cells has not been comprehensively defined. Here we describe the hematopoietic response to ... ...

Abstract	Helminth infections are common in animals. However, the impact of a helminth infection on the function of hematopoietic stem cells (HSCs) and other hematopoietic cells has not been comprehensively defined. Here we describe the hematopoietic response to infection of mice with
Language	English
Publishing date	2023-02-10
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.10.528073
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Article ; Online: Schistosome Infection Impacts Hematopoiesis.

Wijshake, Tobias / Rose, Joseph / Wang, Jipeng / Zielke, Jacob / Marlar-Pavey, Madeleine / Chen, Weina / Collins, James J / Agathocleous, Michalis

Journal of immunology (Baltimore, Md. : 1950)

2024 Volume 212, Issue 4, Page(s) 607–616

Abstract: Helminth infections are common in animals. However, the impact of a helminth infection on the function of hematopoietic stem cells (HSCs) and other hematopoietic cells has not been comprehensively defined. In this article, we describe the hematopoietic ... ...

Abstract	Helminth infections are common in animals. However, the impact of a helminth infection on the function of hematopoietic stem cells (HSCs) and other hematopoietic cells has not been comprehensively defined. In this article, we describe the hematopoietic response to infection of mice with Schistosoma mansoni, a parasitic flatworm that causes schistosomiasis. We analyzed the frequency or number of hematopoietic cell types in the bone marrow, spleen, liver, thymus, and blood and observed multiple hematopoietic changes caused by infection. Schistosome infection impaired bone marrow HSC function after serial transplantation. Functional HSCs were present in the infected liver. Infection blocked bone marrow erythropoiesis and augmented spleen erythropoiesis, observations consistent with the anemia and splenomegaly prevalent in schistosomiasis patients. This work defines the hematopoietic response to schistosomiasis, a debilitating disease afflicting more than 200 million people, and identifies impairments in HSC function and erythropoiesis.
MeSH term(s)	Humans ; Mice ; Animals ; Bone Marrow ; Hematopoietic Stem Cells/metabolism ; Hematopoiesis/physiology ; Erythropoiesis ; Spleen ; Schistosomiasis/complications
Language	English
Publishing date	2024-01-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300195
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Article ; Online: Neutrophil metabolomics in severe COVID-19 reveal GAPDH as a suppressor of neutrophil extracellular trap formation.

Li, Yafeng / Hook, Jessica S / Ding, Qing / Xiao, Xue / Chung, Stephen S / Mettlen, Marcel / Xu, Lin / Moreland, Jessica G / Agathocleous, Michalis

Nature communications

2023 Volume 14, Issue 1, Page(s) 2610

Abstract: Severe COVID-19 is characterized by an increase in the number and changes in the function of innate immune cells including neutrophils. However, it is not known how the metabolome of immune cells changes in patients with COVID-19. To address these ... ...

Abstract	Severe COVID-19 is characterized by an increase in the number and changes in the function of innate immune cells including neutrophils. However, it is not known how the metabolome of immune cells changes in patients with COVID-19. To address these questions, we analyzed the metabolome of neutrophils from patients with severe or mild COVID-19 and healthy controls. We identified widespread dysregulation of neutrophil metabolism with disease progression including in amino acid, redox, and central carbon metabolism. Metabolic changes in neutrophils from patients with severe COVID-19 were consistent with reduced activity of the glycolytic enzyme GAPDH. Inhibition of GAPDH blocked glycolysis and promoted pentose phosphate pathway activity but blunted the neutrophil respiratory burst. Inhibition of GAPDH was sufficient to cause neutrophil extracellular trap (NET) formation which required neutrophil elastase activity. GAPDH inhibition increased neutrophil pH, and blocking this increase prevented cell death and NET formation. These findings indicate that neutrophils in severe COVID-19 have an aberrant metabolism which can contribute to their dysfunction. Our work also shows that NET formation, a pathogenic feature of many inflammatory diseases, is actively suppressed in neutrophils by a cell-intrinsic mechanism controlled by GAPDH.
MeSH term(s)	Humans ; COVID-19/metabolism ; Extracellular Traps/metabolism ; Metabolome ; Metabolomics ; Neutrophils ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism
Chemical Substances	GAPDH protein, human (EC 1.2.1.12) ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) (EC 1.2.1.12)
Language	English
Publishing date	2023-05-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-37567-w
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Article ; Online: The requirement for pyruvate dehydrogenase in leukemogenesis depends on cell lineage.

Jun, Sojeong / Mahesula, Swetha / Mathews, Thomas P / Martin-Sandoval, Misty S / Zhao, Zhiyu / Piskounova, Elena / Agathocleous, Michalis

Cell metabolism

2021 Volume 33, Issue 9, Page(s) 1777–1792.e8

Abstract: Cancer cells are metabolically similar to their corresponding normal tissues. Differences between cancers and normal tissues may reflect reprogramming during transformation or maintenance of the metabolism of the specific normal cell type that originated ...

Abstract	Cancer cells are metabolically similar to their corresponding normal tissues. Differences between cancers and normal tissues may reflect reprogramming during transformation or maintenance of the metabolism of the specific normal cell type that originated the cancer. Here, we compare glucose metabolism in hematopoiesis and leukemia. Thymus T cell progenitors were glucose avid and oxidized more glucose in the tricarboxylic acid cycle through pyruvate dehydrogenase (PDH) as compared with other hematopoietic cells. PDH deletion decreased double-positive T cell progenitor cells but had no effect on hematopoietic stem cells, myeloid progenitors, or other hematopoietic cells. PDH deletion blocked the development of Pten-deficient T cell leukemia, but not the development of a Pten-deficient myeloid neoplasm. Therefore, the requirement for PDH in leukemia reflected the metabolism of the normal cell of origin independently of the driver genetic lesion. PDH was required to prevent pyruvate accumulation and maintain glutathione levels and redox homeostasis.
MeSH term(s)	Cell Lineage ; Citric Acid Cycle ; Humans ; Leukemia ; Oxidoreductases/metabolism ; Pyruvate Dehydrogenase Complex/metabolism ; Pyruvic Acid
Chemical Substances	Pyruvate Dehydrogenase Complex ; Pyruvic Acid (8558G7RUTR) ; Oxidoreductases (EC 1.-)
Language	English
Publishing date	2021-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.07.016
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Article ; Online: Metabolism in physiological cell proliferation and differentiation.

Agathocleous, Michalis / Harris, William A

Trends in cell biology

2013 Volume 23, Issue 10, Page(s) 484–492

Abstract: Stem and progenitor cells proliferate and give rise to other types of cells through differentiation. Deregulation of this process can lead to many diseases including cancer. Recent evidence suggests that an extensive metabolic reconfiguration of cancer ... ...

Abstract	Stem and progenitor cells proliferate and give rise to other types of cells through differentiation. Deregulation of this process can lead to many diseases including cancer. Recent evidence suggests that an extensive metabolic reconfiguration of cancer cells allows them to sustain pathological growth by providing anabolic intermediates for biosynthesis. This raises the question of the physiological role of metabolic pathways during normal cell growth and differentiation. Metabolism changes with differentiation, and metabolic pathways may be controlled by the same signals that control cell proliferation and differentiation. However, metabolism could also reciprocally influence these signals. The role of metabolic regulation may extend beyond the provision of intermediates for the biosynthetic needs of proliferation, to affect cell differentiation. Here we bring together a large number of recent studies that support this suggestion and illustrate some of the mechanisms by which metabolism is linked to cell proliferation and differentiation.
MeSH term(s)	Cell Differentiation ; Cell Proliferation ; Energy Metabolism ; Humans ; Metabolic Networks and Pathways ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction/genetics ; Stem Cells/metabolism ; Stem Cells/pathology
Language	English
Publishing date	2013-06-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2013.05.004
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Article: Metabolism in physiological cell proliferation and differentiation

Agathocleous, Michalis / Harris, William A

Trends in cell biology. 2013 Oct., v. 23, no. 10

2013

Abstract	Stem and progenitor cells proliferate and give rise to other types of cells through differentiation. Deregulation of this process can lead to many diseases including cancer. Recent evidence suggests that an extensive metabolic reconfiguration of cancer cells allows them to sustain pathological growth by providing anabolic intermediates for biosynthesis. This raises the question of the physiological role of metabolic pathways during normal cell growth and differentiation. Metabolism changes with differentiation, and metabolic pathways may be controlled by the same signals that control cell proliferation and differentiation. However, metabolism could also reciprocally influence these signals. The role of metabolic regulation may extend beyond the provision of intermediates for the biosynthetic needs of proliferation, to affect cell differentiation. Here we bring together a large number of recent studies that support this suggestion and illustrate some of the mechanisms by which metabolism is linked to cell proliferation and differentiation.
Keywords	biochemical pathways ; biosynthesis ; cell differentiation ; cell growth ; cell proliferation ; neoplasm cells ; stem cells
Language	English
Dates of publication	2013-10
Size	p. 484-492.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2013.05.004
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Clinical and molecular characteristics associated with Vitamin C deficiency in myeloid malignancies; real world data from a prospective cohort.

Premnath, Naveen / Chung, Stephen S / Weinberg, Olga K / Ikpefan, Ruth / Pandey, Mohak / Kaur, Gurbakhash / Geethakumari, Praveen Ramakrishnan / Afrough, Aimaz / Awan, Farrukh T / Anderson, Larry D / Vusirikala, Madhuri / Collins, Robert H / Chen, Weina / Agathocleous, Michalis / Madanat, Yazan F

Leukemia research

2022 Volume 125, Page(s) 107001

Abstract: Vitamin C is an essential vitamin that acts as a co-factor for many enzymes involved in epigenetic regulation in humans. Low vitamin C levels in hematopoietic stem cells (HSC) promote self-renewal and vitamin C supplementation retards leukaemogenesis in ... ...

Abstract	Vitamin C is an essential vitamin that acts as a co-factor for many enzymes involved in epigenetic regulation in humans. Low vitamin C levels in hematopoietic stem cells (HSC) promote self-renewal and vitamin C supplementation retards leukaemogenesis in vitamin C-deficient mouse models. Studies on vitamin C levels in patients with myeloid malignancies are limited. We thus conducted a retrospective analysis on a prospective cohort of patients with myeloid malignancies on whom plasma vitamin C levels were measured serially at diagnosis and during treatment. Baseline characteristics including hematological indices, cytogenetics, and molecular mutations are described in this cohort. Among 64 patients included in our study, 11 patients (17%) had low vitamin C levels. We noted a younger age at diagnosis for patients with myeloid malignancies who had low plasma vitamin C levels. Patients with low plasma vitamin C levels were more likely to have acute myeloid leukemia compared to other myeloid malignancies. Low vitamin C levels were associated with ASXL1 mutations. Our study calls for further multi-institutional studies to understand the relevance of low plasma vitamin C level in myeloid neoplasms, the role of vitamin C deficiency in leukemogenesis, and the potential benefit of vitamin C supplementation.
MeSH term(s)	Mice ; Animals ; Humans ; Epigenesis, Genetic ; Prospective Studies ; Retrospective Studies ; Myeloproliferative Disorders/genetics ; Mutation ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Ascorbic Acid ; Ascorbic Acid Deficiency/complications ; Ascorbic Acid Deficiency/genetics
Chemical Substances	Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2022-12-21
Publishing country	England
Document type	Letter
ZDB-ID	752396-8
ISSN	1873-5835 ; 0145-2126
ISSN (online)	1873-5835
ISSN	0145-2126
DOI	10.1016/j.leukres.2022.107001
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Article ; Online: Metabolomic profiling of rare cell populations isolated by flow cytometry from tissues.

DeVilbiss, Andrew W / Zhao, Zhiyu / Martin-Sandoval, Misty S / Ubellacker, Jessalyn M / Tasdogan, Alpaslan / Agathocleous, Michalis / Mathews, Thomas P / Morrison, Sean J

eLife

2021 Volume 10

Abstract: ... 000 cells (Agathocleous et al., 2017). Here we describe a new method involving hydrophilic liquid ...

Abstract	Little is known about the metabolic regulation of rare cell populations because most metabolites are hard to detect in small numbers of cells. We previously described a method for metabolomic profiling of flow cytometrically isolated hematopoietic stem cells (HSCs) that detects 60 metabolites in 10,000 cells (Agathocleous et al., 2017). Here we describe a new method involving hydrophilic liquid interaction chromatography and high-sensitivity orbitrap mass spectrometry that detected 160 metabolites in 10,000 HSCs, including many more glycolytic and lipid intermediates. We improved chromatographic separation, increased mass resolution, minimized ion suppression, and eliminated sample drying. Most metabolite levels did not significantly change during cell isolation. Mouse HSCs exhibited increased glycerophospholipids relative to bone marrow cells and methotrexate treatment altered purine biosynthesis. Circulating human melanoma cells were depleted for purine intermediates relative to subcutaneous tumors, suggesting decreased purine synthesis during metastasis. These methods facilitate the routine metabolomic analysis of rare cells from tissues.
MeSH term(s)	Animals ; Chromatography, Liquid/methods ; Female ; Flow Cytometry ; Hydrophobic and Hydrophilic Interactions ; Male ; Mass Spectrometry/methods ; Metabolome ; Metabolomics/methods ; Mice
Language	English
Publishing date	2021-01-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.61980
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Article ; Online: Aspartate availability limits hematopoietic stem cell function during hematopoietic regeneration.

Qi, Le / Martin-Sandoval, Misty S / Merchant, Salma / Gu, Wen / Eckhardt, Matthias / Mathews, Thomas P / Zhao, Zhiyu / Agathocleous, Michalis / Morrison, Sean J

Cell stem cell

2021 Volume 28, Issue 11, Page(s) 1982–1999.e8

Abstract: The electron transport chain promotes aspartate synthesis, which is required for cancer cell proliferation. However, it is unclear whether aspartate is limiting in normal stem cells. We found that mouse hematopoietic stem cells (HSCs) depend entirely on ... ...

Abstract	The electron transport chain promotes aspartate synthesis, which is required for cancer cell proliferation. However, it is unclear whether aspartate is limiting in normal stem cells. We found that mouse hematopoietic stem cells (HSCs) depend entirely on cell-autonomous aspartate synthesis, which increases upon HSC activation. Overexpression of the glutamate/aspartate transporter, Glast, or deletion of glutamic-oxaloacetic transaminase 1 (Got1) each increased aspartate levels in HSCs/progenitor cells and increased the function of HSCs but not colony-forming progenitors. Conversely, deletion of Got2 reduced aspartate levels and the function of HSCs but not colony-forming progenitors. Deletion of Got1 and Got2 eliminated HSCs. Isotope tracing showed aspartate was used to synthesize asparagine and purines. Both contributed to increased HSC function as deletion of asparagine synthetase or treatment with 6-mercaptopurine attenuated the increased function of GLAST-overexpressing HSCs. HSC function is thus limited by aspartate, purine, and asparagine availability during hematopoietic regeneration.
MeSH term(s)	Animals ; Aspartic Acid ; Cell Proliferation ; Hematopoietic Stem Cells ; Mice
Chemical Substances	Aspartic Acid (30KYC7MIAI)
Language	English
Publishing date	2021-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2021.07.011
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Article ; Online: From progenitors to differentiated cells in the vertebrate retina.

Agathocleous, Michalis / Harris, William A

Annual review of cell and developmental biology

2009 Volume 25, Page(s) 45–69

Abstract: Multipotent retinal progenitors undergo a varied number of divisions to produce clones of heterogeneous sizes and cell types. We describe the transition from a proliferating progenitor to a differentiated postmitotic cell and discuss how controls of ... ...

Abstract	Multipotent retinal progenitors undergo a varied number of divisions to produce clones of heterogeneous sizes and cell types. We describe the transition from a proliferating progenitor to a differentiated postmitotic cell and discuss how controls of proliferation operate within individual cells as well as in the whole tissue. We discuss how extracellular and intracellular signaling, transcriptional regulation, cell cycle kinetics, interkinetic nuclear migration, orientation of cell division, and epigenetic modifications all interact to regulate a progenitor's transition from division to differentiation. We also propose some directions for future research.
MeSH term(s)	Animals ; Cell Differentiation ; Humans ; Retina/cytology ; Retina/metabolism ; Stem Cells/cytology ; Stem Cells/metabolism
Language	English
Publishing date	2009
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1293750-2
ISSN	1530-8995 ; 1081-0706
ISSN (online)	1530-8995
ISSN	1081-0706
DOI	10.1146/annurev.cellbio.042308.113259
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