Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LT-HSC re-isolated from tranplants altering the age (young and middle age) of the donor LT-HSC, support cells and recipient mice

ABSTRACT: LT-HSC re-isolated from tranplants altering the age (young and middle age) of the donor LT-HSC, support cells and recipient mice

PROVIDER: PRJNA605371 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11040474.fastq.gz	Fastqsanger.gz
	SRR11040475.fastq.gz	Fastqsanger.gz
	SRR11040476.fastq.gz	Fastqsanger.gz
	SRR11040477.fastq.gz	Fastqsanger.gz
	SRR11040478.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

LT-HSC re-isolated from tranplants altering the age (young and middle age) of the donor LT-HSC, support cells and recipient mice

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.

2020-02-08 | GSE144933 | GEO

LT-HSC from middle-age mice stimulated with IGF1 ATAC-seq

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.

2021-01-12 | GSE164609 | GEO

LT-HSC from young and middle-age mice stimulated with IGF1 RNA-seq

2020-02-08 | GSE144934 | GEO

LT-HSC from young (2mo), middle-age (12mo) and old (22mo) mice for RNA-seq

2020-07-01 | GSE151333 | GEO

LT-HSC from middle-age mice stimulated with IGF1 ATAC-seq

Project description:LT-HSC from middle-age mice stimulated with IGF1 ATAC-seq

| PRJNA691328 | ENA

LT-HSC from young and middle-age mice stimulated with IGF1 RNA-seq

Project description:LT-HSC from young and middle-age mice stimulated with IGF1 RNA-seq

| PRJNA605370 | ENA

Transcription profiling of mouse LT-HSC hematopoietic stem cells from wild type and Cebpa knock-in mutant strains

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

LT-HSC from young (2mo), middle-age (12mo) and old (22mo) mice for RNA-seq

Project description:LT-HSC from young (2mo), middle-age (12mo) and old (22mo) mice for RNA-seq

| PRJNA635499 | ENA

Expression analysis of WASH knockout LT-HSC cells

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.

2014-05-17 | GSE57741 | GEO

Transcription profiling of Pairwise comparisons of purified mouse LT-HSC, ST-HSC and MPP

Project description:Pairwise comparisons of purified mouse LT-HSC, ST-HSC and MPP.

2005-09-09 | E-SMDB-3457 | biostudies-arrayexpress