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ABSTRACT: Mechanisms and Dynamics of Clonal Hematopoiesis of Indeterminate Potential

PROVIDER: PRJNA626680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11576591.fastq.gz	Fastqsanger.gz
	SRR11576591_1.fastq.gz	Fastqsanger.gz
	SRR11576591_2.fastq.gz	Fastqsanger.gz
	SRR11576592.fastq.gz	Fastqsanger.gz
	SRR11576592_1.fastq.gz	Fastqsanger.gz

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Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction

Project description:Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We used a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2-mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. Consistent with age-related clonal hematopoiesis observed in humans, these mice displayed a progressive expansion of Tet2-deficient cells in multiple hematopoietic stem and progenitor cell fractions and blood cell lineages. The expansion of the Tet2-mutant fraction was also observed in bone marrow-derived CCR+ myeloid cell populations within the heart, but there was a negligible impact on the yolk sac-derived CCR2- cardiac resident macrophage population. Transcriptome profiling revealed an enhanced inflammatory signature in the donor-derived macrophages isolated from the heart. Mice receiving Tet2-deficient bone marrow cells spontaneously developed age-related cardiac dysfunction characterized by greater hypertrophy and fibrosis. Altogether, we show that Tet2- mediated hematopoiesis contributes to cardiac dysfunction in a nonconditioned setting that faithfully models the human clonal hematopoiesis in unperturbed bone marrow. Our data support clinical findings that clonal hematopoiesis per se may contribute to diminished health span.

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Nanostring immune profiling of air and cigarette smoke exposed wildtype bone marrow hematopoietic cells and Nanostring immune profiling of air and cigarette smoke exposed bone marrow hematopoietic cells from mice containing Jak2V617F mutant cells

Project description:Extrinsic stressors must have a role in driving clonal hematopoiesis since only a fraction of individuals with clonal hematopoiesis of indeterminate potential (CHIP) develop hematologic malignancy. Smoking behavior is associated with CHIP, but the effects of cigarette smoke on hematopoietic stem cells (HSCs) are unknown. The exploding use of electronic (E)-cigarettes has led to significant concern on their health effects. In this project, we aimed to determine the impact of cigarette smoke on the frequency and numbers of HSCs and inflammatory gene expression changes in bone marrow hematopoietic cells using wildtype mice. We also determined if cigarette smoke drives clonal expansion in mosaic mice containing both wildtype and Jak2V617F mutant cells. We also performed gene expression profiling on the wildtype fraction of bone marrow hematopoietic cells from mosaic mice exposed to cigarette smoke or air to determine if the presence of mutant cells alters the signature of wildtype cells.

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Project description:DNA sequencing of human blood sample for Clonal Hematopoiesis of Indeterminate Potential (CHIP) detection.

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Project description:Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an increased risk of inflammatory conditions, including cardiovascular disease, in humans. The goal of the present data set was to examine the molecular mechanism underlying the increase in inflammation seen with the two most common CHIP mutations, namely loss-of-function mutations in Dnmt3a and Tet2, using murine bone-marrow derived macrophages (BMDM) as a model system.

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