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ABSTRACT: Distribution of Clonal Hematopoiesis of Indeterminate Potential (CHIP) is not associated with Race in Patients with Plasma Cell Neoplasms

PROVIDER: PRJNA856503 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20017100_1.fastq.gz	Fastqsanger.gz
	SRR20017100_2.fastq.gz	Fastqsanger.gz
	SRR20017200_1.fastq.gz	Fastqsanger.gz
	SRR20017200_2.fastq.gz	Fastqsanger.gz
	SRR20017101_1.fastq.gz	Fastqsanger.gz

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Project description:Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A) drive clonal hematopoiesis of indeterminate potential (CHIP) and are associated with adverse prognosis in patients with heart failure (HF). The interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential interaction partners of CHIP-mutated monocytes using combined transcriptomic data from peripheral blood mononuclear cells of HF patients with and without CHIP and cardiac tissue. We demonstrate that DNMT3A inactivation augments macrophage-to-cardiac fibroblasts interactions and induces cardiac fibrosis in mice and humans. Mechanistically, DNMT3A inactivation increases the release of heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) to activate cardiac fibroblasts. These findings not only identify a novel pathway of DNMT3A CHIP-driver mutation-induced instigation and progression of HF, but may also provide a rationale for the development of new anti-fibrotic strategies.

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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

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

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Project description:Background: Patients with JAK2V617F-positive myeloproliferative neoplasms (MPNs) and clonal hematopoiesis of indeterminate potential (CHIP) face a significantly elevated risk of cardiovascular diseases (CVDs). Endothelial cells (ECs) carrying the JAK2V617F mutation have been detected in many MPN patients. In this study, we investigated the molecular basis for the high incidence of cardiovascular complications in MPN patients. Methods: We investigated the impact of endothelial JAK2V617F mutation on CVD development using both transgenic murine models and MPN patient-derived induced pluripotent stem cell lines. Results and Conclusions: Our investigations revealed that JAK2V617F mutant ECs promote CVDs by impairing endothelial function and undergoing endothelial-to-mesenchymal transition (EndMT). Importantly, we discovered that inhibiting the endothelial thrombopoietin receptor MPL suppressed JAK2V617F-induced EndMT and prevented cardiovascular dysfunction caused by mutant ECs. Notably, the endothelial MPL receptor is not essential for the normal physiological regulation of blood cell counts and cardiac function, rendering it a promising therapeutic target for preventing or ameliorating cardiovascular complications in patients with MPNs.

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