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Glycogen accumulation, central carbon metabolism, and aging of hematopoietic stem and progenitor cells.

ABSTRACT: Inspired by recent proteomic data demonstrating the upregulation of carbon and glycogen metabolism in aging human hematopoietic stem and progenitor cells (HPCs, CD34+ cells), this report addresses whether this is caused by elevated glycolysis of the HPCs on a per cell basis, or by a subpopulation that has become more glycolytic. The average glycogen content in individual CD34+ cells from older subjects (>?50 years) was 3.5 times higher and more heterogeneous compared to younger subjects (

SUBMITTER: Poisa-Beiro L

PROVIDER: S-EPMC7360735 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Glycogen accumulation, central carbon metabolism, and aging of hematopoietic stem and progenitor cells.

Poisa-Beiro Laura L Thoma Judith J Landry Jonathan J Sauer Sven S Yamamoto Akihisa A Eckstein Volker V Romanov Natalie N Raffel Simon S Hoffmann Georg F GF Bork Peer P Benes Vladimir V Gavin Anne-Claude AC Tanaka Motomu M Ho Anthony D AD

Scientific reports 20200714 1

Inspired by recent proteomic data demonstrating the upregulation of carbon and glycogen metabolism in aging human hematopoietic stem and progenitor cells (HPCs, CD34+ cells), this report addresses whether this is caused by elevated glycolysis of the HPCs on a per cell basis, or by a subpopulation that has become more glycolytic. The average glycogen content in individual CD34+ cells from older subjects (> 50 years) was 3.5 times higher and more heterogeneous compared to younger subjects (< 35 ye ...[more]

PMID: 32665666

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Project description:BackgroundAccumulation of DNA damage leading to adult stem cell exhaustion has been proposed to be a principal mechanism of aging. Here we tested this hypothesis in healthy individuals of different ages by examining unrepaired DNA double-strand breaks (DSBs) in hematopoietic stem/progenitor cells matured in their physiological microenvironment.Methodology/principal findingsTo asses DNA damage accumulation and repair capacities, ?H2AX-foci were examined before and after exposure to ionizing irradiation. Analyzing CD34+ and CD34- stem/progenitor cells we observed an increase of endogenous ?H2AX-foci levels with advancing donor age, associated with an age-related decline in telomere length. Using combined immunofluorescence and telomere-fluorescence in-situ hybridization we show that ?H2AX-foci co-localize consistently with other repair factors such as pATM, MDC1 and 53BP1, but not significantly with telomeres, strongly supporting the telomere-independent origin for the majority of foci. The highest inter-individual variations for non-telomeric DNA damage were observed in middle-aged donors, whereas the individual DSB repair capacity appears to determine the extent of DNA damage accrual. However, analyzing different stem/progenitor subpopulations obtained from healthy elderly (>70 years), we observed an only modest increase in DNA damage accrual, most pronounced in the primitive CD34+CD38(-)-enriched subfraction, but sustained DNA repair efficiencies, suggesting that healthy lifestyle may slow down the natural aging process.Conclusions/significanceBased on these findings we conclude that age-related non-telomeric DNA damage accrual accompanies physiological stem cell aging in humans. Moreover, aging may alter the functional capacity of human stem cells to repair DSBs, thereby deteriorating an important genome protection mechanism leading to exceeding DNA damage accumulation. However, the great inter-individual variations in middle-aged individuals suggest that additional cell-intrinsic mechanisms and/or extrinsic factors contribute to the age-associated DNA damage accumulation.

Dataset Information

Glycogen accumulation, central carbon metabolism, and aging of hematopoietic stem and progenitor cells.

Publications

Glycogen accumulation, central carbon metabolism, and aging of hematopoietic stem and progenitor cells.

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