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Gene expression profile of HSC/Ps and mature myeloid cells in MDS mutant clone

ABSTRACT: Gene expression profile of HSC/Ps and mature myeloid cells in MDS mutant clone

PROVIDER: PRJNA636975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11915612_1.fastq.gz	Fastqsanger.gz
	SRR11915612_2.fastq.gz	Fastqsanger.gz
	SRR11915613_1.fastq.gz	Fastqsanger.gz
	SRR11915613_2.fastq.gz	Fastqsanger.gz
	SRR11915614_1.fastq.gz	Fastqsanger.gz

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Gene expression profile of HSC/Ps and mature myeloid cells in MDS mutant clone

Project description:MDS are characterized by bone marrow (BM) failure due to ineffective hematopoiesis. However, the underlying mechanisms of ineffective hematopoiesis, in which clonal expansion coexists with accelerated cell death, remain to be elucidated. Recently, we detected CBL exon 8/9 deletion mutation (CBLΔE8/9) in several MDS patients with RUNX1 mutations. The CBLΔE8/9/RUNX1S291fs mice (CR-mice) developed a variety of MDS phenotypes, such as pancytopenia, dysplasia, and ineffective hematopoiesis in BM. RNA-Seq of HSC/progenitor (HSC/P) and mutant mature myeloid BM cells revealed that gene signature induced in the CR-mice is similar to that in MDS patients with BM failure. Especially, innate immune-related genes were significantly dysregulated.

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Gene expression profile of HSC/Ps and mature myeloid cells in HMGA2-OE MDS mutant clone

Project description:Although HMGA2 overexpression (OE) has been reported in several myeloid malignancies, its role in MDS remains unclear. To determine the role of HMGA2 in MDS pathogenesis, we generated MDS mice using patient-derived RUNX1 mutant, and overexpressed HMGA2 in this model. HMGA2-OE MDS mice developed non-infectious pneumonia. Prominent infiltration of neutrophils was observed in the lung tissue. RNA sequencing of HSC/Ps and neutrophils revealed that genes related to platelet activation are significantly activated in HMGA2-OE MDS mice. Flow cytometric analysis showed that P-selectin+ activated platelets tightly interact with neutrophils in the HMGA2-OE MDS mice. Genetic inhibition of P-selectin attenuated neutrophil activation and pneumonia development in the MDS mice. These findings provide new insights into mechanistic basis of systemic complications of MDS.

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Gene expression profile of HSC/Ps and mature myeloid cells in HMGA2-OE MDS mutant clone

Project description:Gene expression profile of HSC/Ps and mature myeloid cells in HMGA2-OE MDS mutant clone

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Gene expression profile of HSC/Ps and mature myeloid cells in Mdivi-1 treated MDS mutant clone

Project description:MDS are characterized by bone marrow (BM) failure due to ineffective hematopoiesis. However, the underlying mechanisms of ineffective hematopoiesis, in which clonal expansion coexists with accelerated cell death, remain to be elucidated. Recently, we detected CBL exon 8/9 deletion mutation (CBLΔE8/9) in several MDS patients with RUNX1 mutations. The CBLΔE8/9/RUNX1S291fs mice (CR-mice) developed a variety of MDS phenotypes, such as pancytopenia, dysplasia, and ineffective hematopoiesis in BM. RNA-Seq of HSC/progenitor (HSC/P) and mutant mature myeloid BM cells revealed that gene signature induced in the CR-mice is similar to that in MDS patients with BM failure. Especially, inflammation and innate immune-related genes were significantly dysregulated. Mdivi-1 treatment significantly attenuated inflammaotry signaling activation and rescued MDS phenotypes.

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MRTF-SRF signaling is required for seeding of HSC/Ps in bone marrow during development

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Project description:Monosomy 7 (-7) and del(7q) are high-risk cytogenetic abnormalities common in myeloid malignancies. We previously reported that CUX1, a homeodomain-containing transcription factor encoded on 7q22, is frequently inactivated in myeloid neoplasms, and CUX1 myeloid tumor suppressor activity is conserved from humans to Drosophila. CUX1-inactivating mutations are recurrent in clonal hematopoiesis of indeterminate potential as well as myeloid malignancies, in which they independently carry a poor prognosis. To determine the role for CUX1 in hematopoiesis, we generated 2 short hairpin RNA-based mouse models with ∼54% (Cux1mid) or ∼12% (Cux1low) residual CUX1 protein. Cux1mid mice develop myelodysplastic syndrome (MDS) with anemia and trilineage dysplasia, whereas CUX1low mice developed MDS/myeloproliferative neoplasms and anemia. In diseased mice, restoration of CUX1 expression was sufficient to reverse the disease. CUX1 knockdown bone marrow transplant recipients exhibited a transient hematopoietic expansion, followed by a reduction of hematopoietic stem cells (HSCs), and fatal bone marrow failure, in a dose-dependent manner. RNA-sequencing after CUX1 knockdown in human CD34+ cells identified a -7/del(7q) MDS gene signature and altered differentiation, proliferative, and phosphatidylinositol 3-kinase (PI3K) signaling pathways. In functional assays, CUX1 maintained HSC quiescence and repressed proliferation. These homeostatic changes occurred in parallel with decreased expression of the PI3K inhibitor, Pik3ip1, and elevated PI3K/AKT signaling upon CUX1 knockdown. Our data support a model wherein CUX1 knockdown promotes PI3K signaling, drives HSC exit from quiescence and proliferation, and results in HSC exhaustion. Our results also demonstrate that reduction of a single 7q gene, Cux1, is sufficient to cause MDS in mice.

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