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Transcriptome analysis of HSPC at 6 days of culture of non- or 20mGy-irradiated LT-HSC

ABSTRACT: Mouse LT-HSC cells were obtained by cytometry sorting, irradiated or not with 20mGy using a GSRD1 (cesium source) and cultured for 6 days in stem cell maintenance medium. HSPCs from these cultures were sorted and RNA extracted for transcriptomic analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE286157 | GEO | 2026/01/13

REPOSITORIES: GEO

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Transcriptome analysis of HSPC at 6 days of culture of non- or 20mGy-irradiated LT-HSC

Project description:Transcriptome analysis of HSPC at 6 days of culture of non- or 20mGy-irradiated LT-HSC

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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.

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