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Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

ABSTRACT: Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

PROVIDER: PRJNA765019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15998200.fastq.gz	Fastqsanger.gz
	SRR15998201_1.fastq.gz	Fastqsanger.gz
	SRR15998201_2.fastq.gz	Fastqsanger.gz
	SRR15998202_1.fastq.gz	Fastqsanger.gz
	SRR15998202_2.fastq.gz	Fastqsanger.gz

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Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

Project description:Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

| PRJNA936438 | ENA

Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

Project description:RNA-sequencing was performed to look for transcriptional differences between wild-type and Mpc2-deficient granulocyte-macrophage progenitors immediately following the deletion of Mpc2. Paper abstract: Hematopoietic stem and progenitor cells likely engage specific metabolic pathways to promote homeostasis of downstream mature lineages. We examined hematopoiesis in mice conditionally deficient in genes required for long-chain fatty acid oxidation (Cpt2), glutaminolysis (Gls), or mitochondrial pyruvate import (Mpc2). Genetic ablation of Cpt2 or Gls minimally impacted most blood lineages. Deletion of Mpc2 led to a sharp decline in mature myeloid cells and a slower reduction in T cells, whereas other hematopoietic lineages were unaffected. Yet MPC2-deficient monocytes and neutrophils rapidly recovered due to a transient increase in proliferation of myeloid but not other progenitors. Competitive bone marrow chimera and stable isotope tracing experiments demonstrated that this proliferative burst was progenitor-intrinsic and accompanied by a metabolic switch to glutaminolysis. Myeloid recovery after loss of MPC2 or cyclophosphamide treatment was delayed in the absence of GLS. Reciprocally, MPC2 was not required for myeloid recovery after cyclophosphamide treatment. Thus, whereas mitochondrial pyruvate metabolism maintains myelopoiesis under steady-state conditions, rapid recovery from acute loss of myeloid cells requires a switch to glutaminolysis in progenitors.

2023-02-22 | GSE225578 | GEO

Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis

Project description:RNA-sequencing was performed to look for transcriptional differences between wild-type and Mpc2-deficient granulocyte-macrophage progenitors. Very few genes were dysregulated in knockout cells relative to wild-type. Gls Mpc2 double knockouts were additionally analyzed to examine extent of Gls and Mpc2 deletion relative to single knockouts. Paper abstract: Hematopoietic homeostasis is maintained by stem and progenitor cells in part by extrinsic feedback cues triggered by mature cell loss. We demonstrate a different mechanism by which hematopoietic progenitors intrinsically anticipate and prevent the loss of mature progeny through metabolic switches. We examined hematopoiesis in mice conditionally deficient in long-chain fatty acid oxidation (carnitine palmitoyltransferase 2, Cpt2), glutaminolysis (glutaminase, Gls), or mitochondrial pyruvate import (mitochondrial pyruvate carrier 2, Mpc2). While genetic ablation of Cpt2 or Gls minimally impacted most blood lineages, deletion of Mpc2 led to a sharp decline in mature myeloid cells. However, MPC2-deficient myeloid cells rapidly recovered due to a transient increase in myeloid progenitor proliferation. Competitive bone marrow chimera and stable isotope tracing experiments demonstrated that this proliferative burst was intrinsic to MPC2-deficient progenitors and accompanied by a metabolic switch to glutaminolysis. Thus, hematopoietic progenitors intrinsically adjust to metabolic perturbations independently of feedback from downstream mature cells to maintain homeostasis.

2021-09-27 | GSE184548 | GEO

Maternal IL-10 restricts fetal emergency myelopoiesis

Project description:Maternal IL-10 restricts fetal emergency myelopoiesis

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Mature B cells and Mesenchymal Stem Cells control emergency myelopoiesis

Project description:Systemic inflammation halts lymphopoiesis and prioritizes myeloid cell production. How blood cell production switches from homeostasis to emergency myelopoiesis is incompletely understood. Here we show that Lymphotoxin-b receptor (LTbR) signaling in combination with TNF and IL1 receptor signaling in mesenchymal stem cells (MSCs) downregulates Il7 expression to shutdown lymphopoiesis during systemic inflammation. LTbR signaling in MSCs also promoted CCL2 production to enable inflammatory monocyte egress from the bone marrow. Furthermore, pharmacological or genetic blocking of Il7 downregulation in MSCs impaired myeloid cell production and egress, which reduced survival against systemic bacterial and viral infections. Interestingly, lymphotoxin a1b2 delivered by B-lineage cells, and specifically by mature B cells, contributed to promote Il7 downregulation and reduce MSC lymphopoietic activity. Our studies revealed an unexpected role for LTbR signaling in MSCs and identified mature B cells as an important regulator of emergency myelopoiesis.

2023-01-20 | GSE218505 | GEO

Interleukin-10 causes interferon γ-dependent emergency myelopoiesis

Project description:Interleukin-10 causes interferon γ-dependent emergency myelopoiesis

| PRJNA721937 | ENA

Interleukin-10 causes interferon-γ-dependent emergency myelopoiesis

Project description:Interleukin-10 causes interferon-γ-dependent emergency myelopoiesis

| PRJNA613303 | ENA

Maternal IL-10 restricts fetal emergency myelopoiesis [scRNA-seq]

Project description:Maternal IL-10 restricts fetal emergency myelopoiesis [scRNA-seq]

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Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

Project description:Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

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Hematopoietic aging promotes cancer by fueling IL-1⍺-driven emergency myelopoiesis

Project description:Age is a major risk factor for cancer, but how aging impacts tumor control remains unclear. Here, we establish that aging of the immune system, regardless of the age of the stroma and tumor, impacts lung cancer progression. Hematopoietic aging enhances emergency myelopoiesis, resulting in the local accumulation of myeloid progenitor-like cells in lung tumors. These cells are a major source of IL-1⍺ that drives the enhanced myeloid response. The age-associated decline of DNMT3A enhances IL-1⍺ production, and disrupting IL-1R1 signaling early during tumor development normalized myelopoiesis and slowed the growth of lung, colonic, and pancreatic tumors. In human tumors, we identified an enrichment for IL-1⍺-expressing monocyte-derived macrophages linked to age, poorer survival, and recurrence, unraveling how aging impacts cancer.

2024-10-23 | GSE275150 | GEO

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