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The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [Young_Elderly_MDS]

ABSTRACT: The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [Young_Elderly_MDS]

PROVIDER: PRJNA759928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15707220.fastq.gz	Fastqsanger.gz
	SRR15707221.fastq.gz	Fastqsanger.gz
	SRR15707222.fastq.gz	Fastqsanger.gz
	SRR15707223.fastq.gz	Fastqsanger.gz
	SRR15707224.fastq.gz	Fastqsanger.gz

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Similar Datasets

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes

Project description:The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes

| PRJNA759927 | ENA

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [overexpression_and_knockdown]

Project description:The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [overexpression_and_knockdown]

| PRJNA759930 | ENA

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [scRNA-Seq]

Project description:The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [scRNA-Seq]

| PRJNA759931 | ENA

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [Young_Elderly_MDS]

Project description:Myelodysplastic syndromes (MDS) are clonal hematopoietic stem cell (HSC) malignancies characterized by ineffective hematopoiesis with increased incidence in elderly individuals. Genetic alterations do not fully explain the molecular pathogenesis of the disease, indicating that other types of lesions may play a role in its development. In this work, we analyzed the transcriptional lesions of human HSCs, demonstrating how aging and MDS are characterized by a complex transcriptional rewiring that manifests as diverse linear and non-linear transcriptional dynamisms. While aging-associated lesions seemed to predispose elderly HSCs to myeloid transformation, disease-specific alterations may be involved in triggering MDS development. Among MDS-specific lesions, we detected the overexpression of the transcription factor (TF) DDIT3. Exogenous upregulation of DDIT3 in human healthy HSCs induced an MDS-like transcriptional state, and a delay in erythropoiesis, with an accumulation of cells in early stages of erythroid differentiation, as determined by single-cell RNA-sequencing. Increased DDIT3 expression was associated with downregulation of transcription factors required for normal erythropoiesis, such as KLF1, TAL1 or SOX6, and with a failure in the activation of their erythroid transcriptional programs. Finally, DDIT3 knockdown in CD34+ cells from MDS patients was able to restore erythropoiesis, as demonstrated by immunophenotypic and transcriptional profiling. These results demonstrate that DDIT3 may be a driver of MDS transformation, and a potential therapeutic target to restore the inefficient erythropoiesis characterizing these patients.

2022-11-10 | GSE183325 | GEO

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [overexpression_and_knockdown]

2022-11-10 | GSE183327 | GEO

The transcription factor DDIT3 is a Potential Driver of Dyserythropoiesis in Myelodysplastic Syndromes [scRNA-Seq]

2022-11-10 | GSE183326 | GEO

ZRSR2 mutant myelodysplastic syndromes

Project description:ZRSR2 mutant myelodysplastic syndromes

| PRJNA671387 | ENA

ZRSR2 mutant myelodysplastic syndromes

Project description:ZRSR2 mutant myelodysplastic syndromes

| PRJNA671388 | ENA

The transcription factor DDIT3 is a potential driver of dyserythropoiesis in myelodysplastic syndromes.

Project description:Myelodysplastic syndromes (MDS) are hematopoietic stem cell (HSC) malignancies characterized by ineffective hematopoiesis, with increased incidence in older individuals. Here we analyze the transcriptome of human HSCs purified from young and older healthy adults, as well as MDS patients, identifying transcriptional alterations following different patterns of expression. While aging-associated lesions seem to predispose HSCs to myeloid transformation, disease-specific alterations may trigger MDS development. Among MDS-specific lesions, we detect the upregulation of the transcription factor DNA Damage Inducible Transcript 3 (DDIT3). Overexpression of DDIT3 in human healthy HSCs induces an MDS-like transcriptional state, and dyserythropoiesis, an effect associated with a failure in the activation of transcriptional programs required for normal erythroid differentiation. Moreover, DDIT3 knockdown in CD34+ cells from MDS patients with anemia is able to restore erythropoiesis. These results identify DDIT3 as a driver of dyserythropoiesis, and a potential therapeutic target to restore the inefficient erythroid differentiation characterizing MDS patients.

| S-EPMC9734135 | biostudies-literature

Oxidative stress in myelodysplastic syndromes

Project description:Control of oxidative stress in the bone marrow (BM) is key for maintaining the balance between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an oxidative stress marker in BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox.

2019-10-30 | PXD013609 | Pride

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