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Updated: Jul 10, 2026

Isolation Method for Long-Term and Short-Term Hematopoietic Stem Cells

Isolation Method for Long-Term and Short-Term Hematopoietic Stem Cells

Published on: May 19, 2023

Hematopoietic stem cell aging and self-renewal.

Brad Dykstra¹, Gerald de Haan

¹Department of Cell Biology, Section Stem Cell Biology, University Medical Center Groningen, University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands. b.j.dykstra@med.umcg.nl

Cell and Tissue Research

|November 17, 2007

Summary

Aging hematopoietic stem cells (HSCs) show functional decline due to intrinsic changes or altered compartment composition. Genetic background significantly influences HSC aging, impacting immune system function.

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Phenotypic Analysis and Isolation of Murine Hematopoietic Stem Cells and Lineage-committed Progenitors

Phenotypic Analysis and Isolation of Murine Hematopoietic Stem Cells and Lineage-committed Progenitors

Published on: July 8, 2012

Area of Science:

Immunology
Hematology
Gerontology

Background:

Organismal aging involves immune system functional decline, largely due to changes in hematopoietic stem cells (HSCs).
Age-dependent alterations in mouse HSCs include increased numbers, reduced homing, and myeloid differentiation bias.
The precise causes of HSC aging, whether intrinsic or extrinsic, and their genetic underpinnings are not fully understood.

Purpose of the Study:

To investigate the mechanisms and genetic basis of age-related changes in hematopoietic stem cells.
To explore the contribution of intrinsic HSC changes versus compartment composition to aging phenotypes.
To leverage genetic diversity in mouse strains to understand HSC aging.

Main Methods:

Analysis of age-dependent changes in HSC numbers, homing efficiency, and differentiation potential in various mouse strains.
Utilizing recombinant inbred strains to map the genetic factors influencing HSC aging.
Investigating gene expression patterns, epigenetic modifications, DNA damage, and reactive oxygen species in aged HSCs.

Main Results:

Identified hallmark age-dependent changes in mouse HSCs, including increased numbers, decreased homing, and myeloid skewing.
Highlighted the significant influence of genetic background on HSC aging characteristics, with notable differences in the C57Bl/6 strain.
Observed coordinated gene expression variations and accumulation of DNA damage and reactive oxygen species in aged HSCs.

Conclusions:

HSC aging is influenced by both intrinsic cellular changes and the surrounding cellular environment.
Genetic factors play a crucial role in determining HSC aging trajectories.
Further research is needed to elucidate whether HSC aging is programmed or stochastic and to determine causality between genetic dysregulation and cellular aging.