Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATAC-seq of VLDLR+ vs VLDLR- HSCs after acute anemia induction

ABSTRACT: ATAC-seq of VLDLR+ vs VLDLR- HSCs after acute anemia induction

PROVIDER: PRJNA1145272 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 28

Similar Datasets

ATAC-seq of VLDLR+ vs VLDLR- HSCs after acute anemia induction

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

The effect of PHZ-induced hemolytic anemia on HSCs [bisulfite-seq]

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

The effect of PHZ-induced hemolytic anemia on HSCs [RNA-seq]

2023-12-04 | GSE178215 | GEO

Vldlr KO vs Jax WT Array

Project description:Analysis of lipid metabolism at gene expression level. Total RNA obtained from isolated retinas from Vldlr ko mice and Jax WT mice

2016-03-14 | E-GEOD-78831 | biostudies-arrayexpress

The effect of PHZ-induced hemolytic anemia on HSCs

Project description:The effect of PHZ-induced hemolytic anemia on HSCs

| PRJNA754382 | ENA

Gene expression data of murine hematopoietic stem cells after anemic stress

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

Reelin and Thrombospondin1 regulate cardiomyocyte proliferation through Vldlr

Project description:We performed RNA-Seq analysis of neoatal rat ventricular cardiomyocytes (NRVCs)which were treated with Reelin,or knocking down Vldlr,Thbs1,or overexpressing Vldlr to investigate the moleclular mechanism of Thbs1/Reelin-Vldlr to regulate cardiomyocyte proliferation.In addition,the day 1mouse cardiomyocytes in Myh6-Cre;Vldlr f/f mice ,Myh6-Cre;Vldlr f/+ mice ,versus Vldlr f/f mice were also performed to explore the fucntion of Vldlr which regulating cardiomyocyte proliferation in vivo.

2021-06-03 | GSE176009 | GEO

The effect of PHZ-induced hemolytic anemia on HSCs [bisulfite-seq]

Project description:The effect of PHZ-induced hemolytic anemia on HSCs [bisulfite-seq]

| PRJNA754388 | ENA

The effect of PHZ-induced hemolytic anemia on HSCs [RNA-seq]

Project description:The effect of PHZ-induced hemolytic anemia on HSCs [RNA-seq]

| PRJNA737763 | ENA

Circular Slc17a5 regulated by VLDLR/QKI pathway inhibits neovascularization

Project description:Investigate whether VLDLR can mediate the biogenesis of circular RNA, and whether an adaptor that bridges the VLDLR signal and the biogenesis of circular RNA .

2025-05-31 | GSE207641 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data