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MRAN expression profiles in mesenchymal progenitor cells freshly-sorted from Wild Type and Lama4-deficient mice

ABSTRACT: mRAN expression profiles in mesenchymal progenitor cells freshly-sorted from Wild Type and Lama4-deficient mice

PROVIDER: PRJNA704574 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13776453.fastq.gz	Fastqsanger.gz
	SRR13776454.fastq.gz	Fastqsanger.gz
	SRR13776455.fastq.gz	Fastqsanger.gz
	SRR13776456.fastq.gz	Fastqsanger.gz
	SRR13776457.fastq.gz	Fastqsanger.gz

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mRAN expression profiles in mesenchymal progenitor cells freshly-sorted from Wild Type and Lama4-deficient mice

Project description:Bone marrow (BM) niche contributes to hematopoietic regeneration under stress like irradiation and leukemia. However, the mechanisms remain poorly defined. We here report that Lama4 deletion in mice results in reduction of mesenchymal progenitors (MPCs) and endothelial cells in BM. Following irradiation, Lama4-/- mice displayed impaired hematopoiesis recovery accompanied with dysregulation of BM niche factors like angiopoietin-1 and Tgfb1 in the MPCs. Post-transplantation of MLL-AF9 acute myeloid leukemia (AML) cells, we observed accelerated AML onset in Lama4-/- mice. Moreover, these Lama4-/- AML mice displayed faster relapse after therapeutic BM transplantation. Mechanistically, Lama4-/- niche promoted AML cell proliferation and chemoresistance to chemotherapy cytarabine by conferring AML greater antioxidant activity. Together, our study demonstrates that Lama4 is required to maintain hematopoietic niche integrity and to suppress AML progression and chemoresistance by restricting metabolic defense support to AML. Therefore, activating Lama4 signaling pathways may offer potential new therapeutic options for AML.

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Expression data from mesenchymal stem and progenitor cells freshly isolated from human bone marrow

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DNA methylation profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs)

Project description:Hematopoietic stem and progenitor cells (HPCs) can be maintained in vitro, but the vast majority of their progeny loses M-bM-^@M-^\stemnessM-bM-^@M-^] during culture. In this study, we have analyzed DNA methylation (DNAm) profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs). DNAm profiles of expanded CD34+ versus CD34- subsets reflected hematopoietic differentiation, whereas culture on TCP or MSCs had little impact. Notably, all cultured HPCs - even those which remained CD34 positive - acquired significant DNA-hypermethylation, particularly in up-stream promoter regions, shore-regions of CpG islands, and binding sides for PU.1 and RUNX1. Our results point to a coordinated epigenetic process which needs to be controlled to enhance self-renewal of HPCs in vitro. 12 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

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DNA methylation profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs)

Project description:Hematopoietic stem and progenitor cells (HPCs) can be maintained in vitro, but the vast majority of their progeny loses “stemness” during culture. In this study, we have analyzed DNA methylation (DNAm) profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs). DNAm profiles of expanded CD34+ versus CD34- subsets reflected hematopoietic differentiation, whereas culture on TCP or MSCs had little impact. Notably, all cultured HPCs - even those which remained CD34 positive - acquired significant DNA-hypermethylation, particularly in up-stream promoter regions, shore-regions of CpG islands, and binding sides for PU.1 and RUNX1. Our results point to a coordinated epigenetic process which needs to be controlled to enhance self-renewal of HPCs in vitro.

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