Transcriptome data of bone marrow hematopoietic stem cells (HSCs) with premature aging
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA868594 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21351040_1.fastq.gz | Fastqsanger.gz | |||
| SRR21351040_2.fastq.gz | Fastqsanger.gz | |||
| SRR21351041_1.fastq.gz | Fastqsanger.gz | |||
| SRR21351041_2.fastq.gz | Fastqsanger.gz | |||
| SRR21351042_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Recent advances have taken advantage of various animal models in HSC aging research, including certain gene mutations, chemicals, and ionizing radiation (IR). To identify the underlying mechanisms and phenotype switching in HSC aging, we employed IR-induced premature HSC aging model and performed RNA-seq of HSCs from the bone marrow (BM) of mice at three months post IR and their age-matched control mice (Ctrl).
2023-08-08 | GSE211007 | GEO
Project description:Bone marrow (BM) is normally maintained in an immune-privileged and anti-inflammatory state, kept in check principally by regulatory T cells (Tregs). Thus, it is reasonable to expect that Tregs will help shield hematopoietic stem cells (HSCs) from excessive inflammation and thereby counteract HSC aging. Understanding how BM Tregs are adapted to the aged BM and whether they are endowed with unique functions to modulate HSC aging will identify targets for prevention of HSC aging. To identify the phenotype switching and function variation in BM Tregs with physiological and premature aging, we performed RNA-seq of Tregs from the bone marrow of mice at three months post irradiation (IR) and their age-matched control mice (Ctrl).
2023-08-08 | GSE211136 | GEO
Project description:Aging of hematopoietic stem cells (HSCs) is associated with the decline of their regenerative capacity, and multi-lineage differentiation potential, contributing to development of blood disorders. The bone marrow microenvironment was recently suggested to influence HSC aging, however the underlying mechanisms remain largely unknown. Here, we show that HSC aging critically depends on bone marrow innervation by the sympathetic nervous system (SNS), as premature loss of SNS nerves or adrenoreceptor b3 (ADRb3) signaling in the microenvironment accelerated the appearance of HSC aging phenotypes reminiscent of physiological aging. Strikingly, supplementation of ADRb3 sympathomimetics to old mice significantly rejuvenated in vivo function of old HSCs, suggesting that the preservation or restitution of SNS innervation during aging may hold the potential for novel HSC rejuvenation strategies.
2018-05-01 | GSE109546 | GEO
Project description:Increasing evidence links metabolic activity and cell growth to decline in hematopoietic stem cell (HSC) function during aging. The Lin28b/Hmga2 pathway controls tissue development and in the hematopoietic system the postnatal downregulation of this pathway causes a decrease in self renewal of adult HSCs compared to fetal HSCs. Igf2bp2 is an RNA binding protein and a mediator of the Lin28b/Hmga2 pathway, which regulates metabolism and growth signaling by influencing RNA stability and translation of its target genes. It is currently unknown whether Lin28/Hmga2/Igf2bp2 signaling impacts on aging-associated impairments in HSC function and hematopoiesis. Here, we analyzed homozygous Igf2bp2 germline knockout mice and wildtype control animals to address this question. The study shows that Igf2bp2 deletion rescues aging phenotypes of the hematopoietic system, such as the expansion of HSC numbers in bone marrow and the biased increase of myeloid cells in peripheral blood. This rescue of hematopoietic aging coincides with reduced mitochondrial metabolism and glycolysis in Igf2bp2-/- HSCs compared to Igf2bp2+/+ HSCs. Conversely, Igf2bp2 overexpression activates protein synthesis pathways in HSCs and leads to a rapid loss of self renewal by enhancing myeloid skewed differentiation in an mTOR/PI3K-dependent manner. Together, these results show that Igf2bp2 regulates energy metabolism and growth signaling in HSCs and that the activity of this pathways influences self renewal, differentiation, and aging of HSCs.
2024-05-21 | PXD018535 | Pride
Project description:Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understand the aging process. Using a model that carries a proofreading defective mitochondrial DNA polymerase, we demonstrate hematopoietic defects reminiscent of premature HSC aging including anemia, lymphopenia and myeloid lineage skewing. However, in contrast to physiologic stem cell aging, rapidly accumulating mitochondrial DNA mutations displayed little involvement of the hematopoietic stem cell pool but rather with distinct differentiation blocks and/or disappearance of downstream progenitors. Hematopoietic stem cells (HSC) has been sorted out from midaged wildtype and mutator mice and compared with stem cells sorted from young and and old wt mice
2011-05-06 | E-GEOD-27686 | biostudies-arrayexpress
Project description:Asrij deletion in mice causes loss of HSC quiescence, myeloid skewing, reduced p53 and increased DNA damage, features attributed to aged hematopoietic stem cells (HSCs). To identify the pathways and processes driving the observed HSC aging-like phenotypes upon asrij depletion and to compare the asrij KO transcriptome with aged wild type HSCs, we performed RNA-seq gene expression profiling of Lin- Sca-1+ c-Kit+ CD150+ CD48- stem cells isolated from asrij KO or asrij floxed (control) mouse bone marrow. Our results identify Asrij as a potential driver of aging-like alterations in HSCs and the RNA-seq based transcriptome could help identify additional aging biomarkers and develop strategies to rejuvenate aged HSCs or prevent premature HSC aging.
2022-01-06 | GSE192948 | GEO
Project description:Insulin-like growth factor-1 (IGF-1) is known as a hematopoietic factor which impacts hematopoietic reconstitution and facilitates thrombopoiesis, although its direct effect on hematopoietic stem cells (HSCs) remains unclear. Here, we show that IGF-1 rapidly prompts megakaryocyte (Mk)-lineage differentiation of HSCs by enhancing mitochondrial activity in HSCs. To identify the phenotype switching and function variation in HSCs with IGF-1 treatment, we performed RNA-seq of HSCs from the bone marrow of mice with single-dose IGF-1 treatment (IGF-1) and their age-matched control mice (Ctrl).
2024-06-05 | GSE229985 | GEO
Project description:Leptin receptor (LEPR) identifies a subpopulation of hematopoietic stem cells (HSCs) with high repopulating potential. In this study, we demonstrated that LEPR-expressing HSCs while exhibiting significantly higher engrafting potential and self-renewing capacity in young mice showed early age-associated decline in these functions as compared to the LEPR- HSCs. LEPR+ HSCs have transcriptomic profiles significantly different from LEPR- HSCs in young mouse bone marrow, but middle-aged HSCs do not have distinct transcriptomic profiles based on LEPR status. The age-related phenotypes were associated with a proinflammatory transcriptomic profile at baseline in young LEPR+ HSCs, which was further exacerbated by age. In contrast, LEPR- HSCs did not show age-associated functional impairment at the ages tested. This suggested that subsets of HSCs are susceptible to age-related decline in function at varying ages and that LEPR+ HSCs are a potential target for early cellular therapeutic interventions in delaying the detrimental effects of aging in hematopoiesis.
2023-02-18 | GSE221126 | GEO
Project description:During aging, hematopoietic stem cell (HSC) function progressively declines which can lead to reduced blood cell production and regeneration, impaired lymphoid cell production and ineffective erythropoiesis. In this study, we uncovered that during aging the cell surface presentation of the type-1 transmembrane protein P-selectin (CD62P, encoded by Selp) increases in a large fraction of HSCs. Notably, expression of P-selectin molecularly and functionally dichotomized the aging HSC pool; stem cells presenting with high abundance of P-selectin were hallmarked by aging-associated gene expression programs and reduced repopulation upon regenerative stress. Overexpression of Selp in young HSCs was sufficient to impair long-term reconstitution potential and repress erythropoiesis. Moreover, IL-1β, which is chronically elevated in the aged bone marrow, triggered Selp expression in HSCs. The aged transcriptome, including Selp, was largely restored when aged HSCs were transplanted to young mice. Mechanistically, we uncovered that appropriate stimulation of P-selectin by its primary ligand, P-selectin glycoprotein ligand-1 (PSGL-1), suppressed aging-associated gene expression and reversely, lack of P-selectin signaling led to HSC premature aging. Collectively, our study uncovered a novel functional role of P-selectin engagement in regulating HSC regeneration and driving stem cell aging when perturbed.
2025-03-21 | GSE269360 | GEO
Project description:To determine how aging impacts gene expression in hematopoietic stem cells (HSCs), human CD34+ cells from bone marrow (34BM) and mobilized stem cell products (34P38NPBSC) were examined using microarray-based expression profiling. Differential expression changes were confirmed by microarray comparisons of younger and older expanded T-cell populations.
2008-12-01 | GSE13496 | GEO