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Hematopoietic Stem Cell Heterogeneity in JAK2 V617F+ Essential Thrombocythemia

ABSTRACT: Hematopoietic Stem Cell Heterogeneity in JAK2 V617F+ Essential Thrombocythemia

PROVIDER: PRJNA436952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6806620_1.fastq.gz	Fastqsanger.gz
	SRR6806620_2.fastq.gz	Fastqsanger.gz
	SRR6806630_1.fastq.gz	Fastqsanger.gz
	SRR6806630_2.fastq.gz	Fastqsanger.gz
	SRR6806621_1.fastq.gz	Fastqsanger.gz

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Hematopoietic Stem Cell Heterogeneity in JAK2 V617F+ Essential Thrombocythemia

Project description:In this study, we explored the transcriptome of hematopoietic stem cells (HSCs) and megakaryocyte-erythroid progenitors (MEPs) in JAK2 V617F+ PV and ET and found that distinctive gene expression patterns within MPN subtypes begin at the HSC stage. HSCs from ET exhibited prominent megakaryocyte (Mk)-lineage priming. The differentially expressed genes (DEGs) indicated that cellular processes and signaling pathways in HSCs and MEPs from healthy donors (HDs), PV and ET patients are differentially modulated

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DNMT3A R882H mutation in JAK2 V617F AML cell line SET-2

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Effects of the treatment with pegIFNa, Azacytidine or pegIFNa+Azacytidine in LT-HSCs from JAK2-V617F MPN mice or JAK2-V617F;Dnmt3a-KO MPN mice.

Project description:Pegylated interferon alpha (pegIFNα) can induce molecular remissions in JAK2-V617F-positive myeloproliferative neoplasms (MPN) patients by targeting long-term hematopoietic stem cells (LT-HSCs). Additional somatic mutations in genes regulating LT-HSC self-renewal, such as DNMT3A, have been reported to have poorer responses to pegIFNα. We investigated if DNMT3A loss leads to alterations in JAK2-V617F LT-HSCs functions conferring resistance to pegIFNα treatment in a mouse model of MPN and in hematopoietic progenitors from MPN patients. Long-term treatment with pegIFNα normalized blood parameters, reduced splenomegaly and JAK2-V617F-chimerism in single-mutant JAK2-V617F (VF) mice. However, pegIFNα in VF;Dnmt3aΔ/Δ (VF;DmΔ/Δ) mice worsened splenomegaly and failed to reduce JAK2-V617F-chimerism. Furthermore, LT-HSCs from VF;DmΔ/Δ mice compared to VF were less prone to accumulate DNA damage and exit dormancy upon pegIFNα treatment. RNA-sequencing showed that IFNα induced stronger upregulation of inflammatory pathways in LT-HSCs from VF;DmΔ/Δ compared to VF mice, indicating that the resistance of VF;DmΔ/Δ LT-HSC was not due to failure in IFNα signaling. Transplantations of bone marrow from pegIFNα treated VF;DmΔ/Δ mice gave rise to more aggressive disease in secondary and tertiary recipients. Liquid cultures of hematopoietic progenitors from MPN patients with JAK2-V617F and DNMT3A mutation showed increased percentages of JAK2-V617F-positive colonies upon IFNα exposure, whereas in patients with JAK2-V617F alone the percentages of JAK2-V617F-positive colonies decreased or remained unchanged. PegIFNα combined with 5-azacytidine only partially overcame resistance in VF;DmΔ/Δ mice. However, this combination strongly decreased the JAK2-mutant allele burden in mice carrying VF mutation only, showing potential to inflict substantial damage preferentially to the JAK2-mutant clone.

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