ATAC-seq of VLDLR+ vs VLDLR- HSCs after acute anemia induction
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ABSTRACT:
PROVIDER: PRJNA1145272 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30161286_1.fastq.gz | Fastqsanger.gz | |||
| SRR30161286_2.fastq.gz | Fastqsanger.gz | |||
| SRR30161287_1.fastq.gz | Fastqsanger.gz | |||
| SRR30161287_2.fastq.gz | Fastqsanger.gz | |||
| SRR30161288_1.fastq.gz | Fastqsanger.gz |
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Project description:Hematopoietic stem cells (HSCs) react to various stress conditions. However, it is unclear whether and how HSCs respond to severe anemia. Here, we demonstrate that upon induction of acute anemia, HSCs rapidly proliferate and enhance their erythroid differentiation potential. In severe anemia, lipoprotein profiles largely change and the concentration of ApoE increases. In HSCs, transcription levels of lipid metabolism-related genes, such as very low-density lipoprotein receptor (Vldlr), are upregulated. Stimulation of HSCs with ApoE enhances their erythroid potential, whereas HSCs in Apoe knockout mice do not respond to anemia induction. VldlrhighHSCs show higher erythroid potential, which is enhanced after acute anemia induction. VldlrhighHSCs are epigenetically distinct because of their low chromatin accessibility, and more chromatin regions are closed upon acute anemia induction. Chromatin regions closed upon acute anemia induction are mainly binding sites of Erg. Inhibition of Erg enhanced the erythroid differentiation potential of HSCs. Our findings indicate that lipoprotein metabolism plays a crucial role in HSC regulation under severe anemic conditions.
2024-08-07 | GSE274144 | GEO
Project description:Hematopoietic stem cells (HSCs) are capable of regenerating the blood system, but the instructive cues that direct HSCs to regenerate particular lineages lost to the injury remain elusive. Here, we show that iron is increasingly taken up by HSCs during anemia and induces erythroid gene expression and regeneration in a Tet2-dependent manner. Lineage tracing of HSCs revealed that HSCs respond to hemolytic anemia by increasing erythroid output. The number of HSCs in the spleen, but not bone marrow, increased upon anemia and these HSCs exhibited enhanced proliferation, erythroid differentiation, iron uptake, and TET2 protein expression. Increased iron in HSCs promoted DNA demethylation and expression of erythroid genes. Suppressing iron uptake or TET2 expression impaired erythroid genes expression and erythroid differentiation of HSCs; iron supplementation, however, augmented these processes. These results establish that the physiological level of iron taken up by HSCs has an instructive role in promoting erythroid-biased differentiation of HSCs.
2023-12-04 | GSE182058 | GEO
Project description:Hematopoietic stem cells (HSCs) are capable of regenerating the blood system, but the instructive cues that direct HSCs to regenerate particular lineages lost to the injury remain elusive. Here, we show that iron is increasingly taken up by HSCs during anemia and induces erythroid gene expression and regeneration in a Tet2-dependent manner. Lineage tracing of HSCs revealed that HSCs respond to hemolytic anemia by increasing erythroid output. The number of HSCs in the spleen, but not bone marrow, increased upon anemia and these HSCs exhibited enhanced proliferation, erythroid differentiation, iron uptake, and TET2 protein expression. Increased iron in HSCs promoted DNA demethylation and expression of erythroid genes. Suppressing iron uptake or TET2 expression impaired erythroid genes expression and erythroid differentiation of HSCs; iron supplementation, however, augmented these processes. These results establish that the physiological level of iron taken up by HSCs has an instructive role in promoting erythroid-biased differentiation of HSCs.
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Project description:The effect of PHZ-induced hemolytic anemia on HSCs
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Project description:Adult hematopoietic stem cells (HSCs) react to various stress conditions by rapidly proliferating and preferentially differentiating towards desired cell types. However, it is unclear whether and how HSCs respond to severe anemic conditions. Here we demonstrate that HSCs rapidly proliferate and enhance their erythroid potential upon induction of acute anemia. Under severe anemic conditions, the concentration of erythropoietin (EPO) does not increase in the bone marrow. Instead, lipoprotein profiles largely changed, and the concentration of apolipoprotein E (ApoE) increased. In HSCs, transcription levels of lipid metabolism-related genes such as very low-density lipoprotein receptor (Vldlr) were significantly up-regulated. Stimulation of HSCs with recombinant ApoE enhanced the erythroid potential, while HSCs of ApoE knockout mice did not respond to the hemolysis induction. We also found that VLDLRhighHSCs have higher erythroid differentiation potential, particularly after acute anemia induction. VLDLRhighHSCs were epigenetically distinct from VLDLRlowHSCs, as their chromatin accessibility was lower and more chromatin regions were closed upon acute anemia induction. Finally, we identified that the chromatin regions closed upon the acute anemia induction were mainly binding sites of a transcription factor Erg. Treatment of HSC with Erg inhibitor enhanced erythroid differentiation potential, as seen in the ApoE treatment. Our findings indicate that lipoprotein metabolism, particularly ApoE, plays a crucial role in HSC regulation under severe anemia conditions in a non-canonical fashion, unlike a conventional factor such as EPO.
2023-06-30 | GSE212392 | GEO
Project description:The effect of PHZ-induced hemolytic anemia on HSCs [RNA-seq]
| PRJNA737763 | ENA
Project description:The effect of PHZ-induced hemolytic anemia on HSCs [bisulfite-seq]
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Project description:Compromised renal function after renal allograft transplantation often results in anemia in the recipient. Molecular mechanisms leading to anemia during acute rejection are not fully understood; inadequate erythropoietin production and iron deficiency have been reported to be the main contributors. To increase our understanding of the molecular events underlying anemia in acute rejection, we analyzed the gene expression profiles of peripheral blood lymphocytes (PBL) from four pediatric renal allograft recipients with acute rejection and concurrent anemia, using DNA microarrays containing 9000 human cDNA clones (representing 7469 unique genes). In these anemic rejecting patients, an 'erythropoiesis cluster' of 11 down-regulated genes was identified, involved in hemoglobin transcription and synthesis, iron and folate binding and transport. Additionally, some alloimmune response genes were simultaneously down-regulated. An independent data set of 36 PBL samples, some with acute rejection and some with concurrence of acute rejection and anemia, were analyzed to support a possible association between acute rejection and anemia. In conclusion, analysis using DNA microarrays has identified a cluster of genes related to hemoglobin synthesis and/or erythropoeisis that was altered in kidneys with renal allograft rejection compared with normal kidneys. The possible relationship between alterations in the expression of this cluster, reduced renal function, the alloimmune process itself, and other influences on the renal transplant awaits further analysis. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Keywords: disease_state_design
2006-01-06 | GSE3976 | GEO