Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Diminishing potential to replace damaged tissues is a hallmark for ageing of somatic stem cells, but the mechanisms remain elusive. Here, we present proteome-wide atlases of age-associated alterations in human haematopoietic stem and progenitor cells (HPCs) and five other cell populations that constitute the bone marrow niche. For each, the abundance of a large fraction of the ~12,000 proteins identified is assessed in 59 human subjects from different ages. As the HPCs become older, pathways in central carbon metabolism exhibit features reminiscent of the Warburg effect, where glycolytic intermediates are rerouted towards anabolism. Simultaneously, altered abundance of early regulators of HPC differentiation reveals a reduced functionality and a bias towards myeloid differentiation. Ageing causes alterations in the bone marrow niche too, and diminishes the functionality of the pathways involved in HPC homing. The data represent a valuable resource for further analyses, and for validation of knowledge gained from animal models.

Original publication

DOI

10.1038/s41467-018-06353-4

Type

Journal article

Journal

Nat Commun

Publication Date

01/10/2018

Volume

9

Keywords

Adult, Adult Stem Cells, Aging, Bone Marrow Cells, Carbon, Cellular Senescence, Female, Gene Expression Profiling, Glycolysis, Hematopoiesis, Hematopoietic Stem Cells, Humans, Male, Middle Aged, Proteome, Stem Cell Niche, Young Adult