A canonical to non-canonical Wnt signalling switch in haematopoietic stem-cell ageing

  • Maria Carolina Florian
  • , Kalpana J. Nattamai
  • , Karin Dörr
  • , Gina Marka
  • , Bettina Überle
  • , Virag Vas
  • , Christina Eckl
  • , Immanuel Andrä
  • , Matthias Schiemann
  • , Robert A.J. Oostendorp
  • , Karin Scharffetter-Kochanek
  • , Hans Armin Kestler
  • , Yi Zheng
  • , Hartmut Geiger

Research output: Contribution to journalArticlepeer-review

266 Scopus citations

Abstract

Many organs with a high cell turnover (for example, skin, intestine and blood) are composed of short-lived cells that require continuous replenishment by somatic stem cells. Ageing results in the inability of these tissues to maintain homeostasis and it is believed that somatic stem-cell ageing is one underlying cause of tissue attrition with age or age-related diseases. Ageing of haematopoietic stem cells (HSCs) is associated with impaired haematopoiesis in the elderly. Despite a large amount of data describing the decline of HSC function on ageing, the molecular mechanisms of this process remain largely unknown, which precludes rational approaches to attenuate stem-cell ageing. Here we report an unexpected shift from canonical to non-canonical Wnt signalling in mice due to elevated expression of Wnt5a in aged HSCs, which causes stem-cell ageing. Wnt5a treatment of young HSCs induces ageing-associated stem-cell apolarity, reduction of regenerative capacity and an ageing-like myeloid-lymphoid differentiation skewing via activation of the small Rho GTPase Cdc42. Conversely, Wnt5a haploinsufficiency attenuates HSC ageing, whereas stem-cell-intrinsic reduction of Wnt5a expression results in functionally rejuvenated aged HSCs. Our data demonstrate a critical role for stem-cell-intrinsic non-canonical Wnt5a signalling in HSC ageing.

Original languageEnglish
Pages (from-to)392-396
Number of pages5
JournalNature
Volume503
Issue number7476
DOIs
StatePublished - 2013

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