Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline

Marco L. Hennrich, Natalie Romanov, Patrick Horn, Samira Jaeger, Volker Eckstein, Violetta Steeples, Fei Ye, Ximing Ding, Laura Poisa-Beiro, Mang Ching Lai, Benjamin Lang, Jacqueline Boultwood, Thomas Luft, Judith B. Zaugg, Andrea Pellagatti, Peer Bork, Patrick Aloy, Anne-Claude Gavin () and Anthony D. Ho ()
Additional contact information
Marco L. Hennrich: Structural and Computational Biology Unit
Natalie Romanov: Structural and Computational Biology Unit
Patrick Horn: Molecular Medicine Partnership Unit (MMPU)
Samira Jaeger: The Barcelona Institute of Science and Technology
Volker Eckstein: Heidelberg University
Violetta Steeples: University of Oxford and Oxford BRC Haematology Theme
Fei Ye: Structural and Computational Biology Unit
Ximing Ding: Structural and Computational Biology Unit
Laura Poisa-Beiro: Molecular Medicine Partnership Unit (MMPU)
Mang Ching Lai: Structural and Computational Biology Unit
Benjamin Lang: Structural and Computational Biology Unit
Jacqueline Boultwood: University of Oxford and Oxford BRC Haematology Theme
Thomas Luft: Heidelberg University
Judith B. Zaugg: Structural and Computational Biology Unit
Andrea Pellagatti: University of Oxford and Oxford BRC Haematology Theme
Peer Bork: Structural and Computational Biology Unit
Patrick Aloy: The Barcelona Institute of Science and Technology
Anne-Claude Gavin: Structural and Computational Biology Unit
Anthony D. Ho: Molecular Medicine Partnership Unit (MMPU)

Nature Communications, 2018, vol. 9, issue 1, 1-18

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-06353-4

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