RNA-Seq analysis of LT-HSC isolated from fetal liver and adult bone marrow.
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB11735 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1121786_1.fastq.gz | Fastqsanger.gz | |||
| ERR1121786_2.fastq.gz | Fastqsanger.gz | |||
| ERR1121787_1.fastq.gz | Fastqsanger.gz | |||
| ERR1121787_2.fastq.gz | Fastqsanger.gz | |||
| ERR1121788_1.fastq.gz | Fastqsanger.gz |
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Project description:We isolated murine fetal liver and murine adult bone marrow and FACS sorted LT-HSCs, ST-HSCs and MPPs. We used global expression analysis by microarray to compare regulated genesets in different HSC populations in fetal and adult.
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Project description:Hematopoietic stem cells (HSC) has unique characteristic to self-renew and replenish the entire blood system. During development, HSCs originate in the aorta-gonads-mesonephros (AGM), from where they migrate into the fetal liver at E11. Once resided in fetal liver HSC proliferate extensively to make sufficient stem pool for adult life. Around birth, HSC from FL migrate to bone marrow (BM) which is major site of hematopoiesis for whole adult life. In contrast to FL HSC, BM HSC remain quiescence state and give rise to different blood cell type under normal homeostatic condition. It has shown that FL HSCs display significantly faster expansion kinetics when transplanted into lethally irradiate mice, compared with HSCs from adult BM. However, detail molecular mechanism behind the difference in self-renewal potential is not fully understood. Here, we present the genome-wide transcriptome analysis of more proliferative FL HSC compared to quiescent BM HSC using RNA-Seq platform.
2016-02-19 | E-MTAB-4034 | biostudies-arrayexpress
Project description:Long-term hematopoietic stem cells (LT-HSCs) are responsible for lifelong maintenance and regeneration of the blood system. Loss of LT-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased rate of infection, poor vaccination response, and increased risk of hematologic malignancies. While cellular and molecular hallmarks of LT-HSC aging have been defined1-3, a barrier to achieving the goal of extending healthy hematopoietic function into older age is the lack of understanding of the nature and timing of the initiating events that cause LT-HSC aging. Here we show that hallmarks of LT-HSC aging and decline in hematopoietic function accumulate by middle age in mice, and that the hematopoietic cell-extrinsic bone marrow (BM) microenvironment at middle age is necessary and sufficient to cause LT-HSC aging. Using unbiased transcriptome-based approaches, we identify decreased production of IGF1 by mesenchymal stromal cells (MSC) in the local middle-aged BM microenvironment as a factor causing LT-HSC aging and show that direct stimulation of middle-aged LT-HSCs with IGF1 rescues hallmarks of aging. Together, our study demonstrates that the initiating events causing LT-HSC and hematopoietic aging emerge by middle age and are caused by hematopoietic cell-extrinsic changes in the BM microenvironment. Declining IGF1 in the BM microenvironment at middle age represents a compelling target for intervention using prophylactic therapies to effectively extend healthspan and prevent decline in hematopoietic function during aging.
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Project description:Gene expression of LT-HSC (CD150+Flt3-lin-Sca-Kit+) hematopoietic stem cells from wild type mice was compared with LT-HSC from Cebpa knock-in mutant mice (K/L mutants). Fetal liver cells for each genotype were competitively transplanted into irradiant recipients. Donor-derived LT-HSC cells were isolated by FACS sorting of recipient bone marrow. Biological replicates of each (3 for wt, 2 for K/L) were generated and expression profiles were determined by hybridization to Affymetrix Moe430_2 arrays.
2009-11-03 | E-TABM-694 | biostudies-arrayexpress
Project description:The transcriptome of LT-HSC (CD34+CD38-CD45RA+CD90+CD49f+) and ST-HSC (CD34+CD38-CD45RA+CD90-CD49f-) from healthy adult human Bone Marrow Cells were assessed by RNA-seq.
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Project description:Long-term hematopoietic stem cells (LT-HSCs) are responsible for lifelong maintenance and regeneration of the blood system. Loss of LT-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased rate of infection, poor vaccination response, and increased risk of hematologic malignancies. While cellular and molecular hallmarks of LT-HSC aging have been defined, a barrier to achieving the goal of extending healthy hematopoietic function into older age is the lack of understanding of the nature and timing of the initiating events that cause LT-HSC aging. Here we show that hallmarks of LT-HSC aging and decline in hematopoietic function accumulate by middle age in mice, and that the hematopoietic cell-extrinsic bone marrow (BM) microenvironment at middle age is necessary and sufficient to cause LT-HSC aging. Using unbiased transcriptome-based approaches, we identify decreased production of IGF1 by mesenchymal stromal cells (MSC) in the local middle-aged BM microenvironment as a factor causing LT-HSC aging and show that direct stimulation of middle-aged LT-HSCs with IGF1 rescues hallmarks of aging. Together, our study demonstrates that the initiating events causing LT-HSC and hematopoietic aging emerge by middle age and are caused by hematopoietic cell-extrinsic changes in the BM microenvironment. Declining IGF1 in the BM microenvironment at middle age represents a compelling target for intervention using prophylactic therapies to effectively extend healthspan and prevent decline in hematopoietic function during aging.
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Project description:Long-term hematopoietic stem cells (LT-HSCs) are responsible for lifelong maintenance and regeneration of the blood system. Loss of LT-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased rate of infection, poor vaccination response, and increased risk of hematologic malignancies. While cellular and molecular hallmarks of LT-HSC aging have been defined1-3, a barrier to achieving the goal of extending healthy hematopoietic function into older age is the lack of understanding of the nature and timing of the initiating events that cause LT-HSC aging. Here we show that hallmarks of LT-HSC aging and decline in hematopoietic function accumulate by middle age in mice, and that the hematopoietic cell-extrinsic bone marrow (BM) microenvironment at middle age is necessary and sufficient to cause LT-HSC aging. Using unbiased transcriptome-based approaches, we identify decreased production of IGF1 by mesenchymal stromal cells (MSC) in the local middle-aged BM microenvironment as a factor causing LT-HSC aging and show that direct stimulation of middle-aged LT-HSCs with IGF1 rescues hallmarks of aging. Together, our study demonstrates that the initiating events causing LT-HSC and hematopoietic aging emerge by middle age and are caused by hematopoietic cell-extrinsic changes in the BM microenvironment. Declining IGF1 in the BM microenvironment at middle age represents a compelling target for intervention using prophylactic therapies to effectively extend healthspan and prevent decline in hematopoietic function during aging.
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Project description:A 2 Gy-total body irradiation (TBI) of WT mice induces a second wave of ROS and a second wave of apoptosis in hematopoietic stem cells starting from 6 days after irradiation. In CD169DTR/+ mice, which are depleted in CD169+ resident macrophages after a diphtheria toxin injection, these two waves do not occur and a total recovery of the LT-HSC pool is observed, contrarily to the LT-HSC pool from WT mice, which is decreased. Our goal is to understand why these secondary waves of apoptosis and ROS occur in LT-HSC from irradiated WT mice and not in LT-HSC from irradiated mice depleted in resident macrophages, allowing a recovery of the LT-HSC pool. We used microarrays to compare the global gene expression in LT-HSC isolated from WT and CD169DTR/+ mice 5 days after irradiation, i.e. just before both secondary waves of ROS and apoptosis occurred in WT mice.
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Project description:Long-term hematopoietic stem cells (LT-HSCs) are responsible for lifelong maintenance and regeneration of the blood system. Loss of LT-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased rate of infection, poor vaccination response, and increased risk of hematologic malignancies. While cellular and molecular hallmarks of LT-HSC aging have been defined1-3, a barrier to achieving the goal of extending healthy hematopoietic function into older age is the lack of understanding of the nature and timing of the initiating events that cause LT-HSC aging. Here we show that hallmarks of LT-HSC aging and decline in hematopoietic function accumulate by middle age in mice, and that the hematopoietic cell-extrinsic bone marrow (BM) microenvironment at middle age is necessary and sufficient to cause LT-HSC aging. Using unbiased transcriptome-based approaches, we identify decreased production of IGF1 by mesenchymal stromal cells (MSC) in the local middle-aged BM microenvironment as a factor causing LT-HSC aging and show that direct stimulation of middle-aged LT-HSCs with IGF1 rescues hallmarks of aging. Together, our study demonstrates that the initiating events causing LT-HSC and hematopoietic aging emerge by middle age and are caused by hematopoietic cell-extrinsic changes in the BM microenvironment. Declining IGF1 in the BM microenvironment at middle age represents a compelling target for intervention using prophylactic therapies to effectively extend healthspan and prevent decline in hematopoietic function during aging.
2020-07-01 | GSE151333 | GEO
Project description:Investigation of whole genome gene expression level changes in WASH knockout LT-HSCs, compared to the WASH WT strain. To find the reason that causes LT-HSC abnormal.
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