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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE132683 | GEO | 2021/12/29

REPOSITORIES: GEO

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells.

Project description:[Figure: see text].

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

Project description:We collected significant amount of phenotypic and mechanistic data from a ATF4 knockout mouse model and demonstrated that HSC defects with an aging-like phenotype (expanded pool of phenotypical HSCs, decreased number of functional HSCs, impaired repopulating and self-renewal capacities of HSCs and myeloid bias) occurred in the ATF4 KO mice, suggesting that not only ATF4 indeed represents a pivotal factor for adult HSC function but also we had successfully constructed an ideal and attractive model to study aging and aging-related disease.

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

Project description:Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

Project description:Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

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Project description:Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

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ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Bcl11a Deficiency Leads to Hematopoietic Stem Cell Defects with an Aging-like Phenotype.

Project description:B cell CLL/lymphoma 11A (BCL11A) is a transcription factor and regulator of hemoglobin switching that has emerged as a promising therapeutic target for sickle cell disease and thalassemia. In the hematopoietic system, BCL11A is required for B lymphopoiesis, yet its role in other hematopoietic cells, especially hematopoietic stem cells (HSCs) remains elusive. The extensive expression of BCL11A in hematopoiesis implicates context-dependent roles, highlighting the importance of fully characterizing its function as part of ongoing efforts for stem cell therapy and regenerative medicine. Here, we demonstrate that BCL11A is indispensable for normal HSC function. Bcl11a deficiency results in HSC defects, typically observed in the aging hematopoietic system. We find that downregulation of cyclin-dependent kinase 6 (Cdk6), and the ensuing cell-cycle delay, correlate with HSC dysfunction. Our studies define a mechanism for BCL11A in regulation of HSC function and have important implications for the design of therapeutic approaches to targeting BCL11A.

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Project description:Somatic loss-of-function mutations in the ten-eleven translocation 2 (TET2) gene occur in a significant proportion of patients with myeloid malignancies. Although there are extensive genetic data implicating TET2 mutations in myeloid transformation, the consequences of Tet2 loss in hematopoietic development have not been delineated. We report here an animal model of conditional Tet2 loss in the hematopoietic compartment that leads to increased stem cell self-renewal in vivo as assessed by competitive transplant assays. Tet2 loss leads to a progressive enlargement of the hematopoietic stem cell compartment and eventual myeloproliferation in vivo, including splenomegaly, monocytosis, and extramedullary hematopoiesis. In addition, Tet2(+/-) mice also displayed increased stem cell self-renewal and extramedullary hematopoiesis, suggesting that Tet2 haploinsufficiency contributes to hematopoietic transformation in vivo.

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Attrition of X Chromosome Inactivation in Aged Hematopoietic Stem Cells.

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