☆ 4.8 Article

Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2014)

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Journal

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 29, Pages 10592-10597

Publisher

NATL ACAD SCIENCES
DOI: 10.1073/pnas.1405546111

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Multidisciplinary Sciences

Funding

  1. French government [ANR-12-BSV1-0001-01]
  2. Ligue contre le Cancer (Grand Est)
  3. Association pour la Recherche sur le Cancer
  4. Cent Pour Sang La Vie
  5. Conseil Regional de Bourgogne (CRB)
  6. National Research Agency under the program Investissements d'Avenir (LipSTIC Labex) [ANR-11-LABX-0021]
  7. National Research Agency
  8. CRB
  9. Institut National de la Sante et de la Recherche Medicale (INSERM)/CRB
  10. INSERM/CRB
  11. Societe Francaise d'Hematologie
  12. Agence Nationale de la Recherche (ANR) [ANR-12-BSV1-0001] Funding Source: Agence Nationale de la Recherche (ANR)

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The hematopoietic system declines with age. Myeloid-biased differentiation and increased incidence of myeloid malignancies feature aging of hematopoietic stem cells (HSCs), but the mechanisms involved remain uncertain. Here, we report that 4-mo-old mice deleted for transcription intermediary factor 1 gamma (Tif1 gamma) in HSCs developed an accelerated aging phenotype. To reinforce this result, we also show that Tif1 gamma is down-regulated in HSCs during aging in 20-mo-old wild-type mice. We established that Tif1 gamma controls TGF-beta 1 receptor (Tgfbr1) turnover. Compared with young HSCs, Tif1 gamma(-/-) and old HSCs are more sensitive to TGF-beta signaling. Importantly, we identified two populations of HSCs specifically discriminated by Tgfbr1 expression level and provided evidence of the capture of myeloid-biased (Tgfbr1(hi)) and myeloid-lymphoid-balanced (Tgfbr1(lo)) HSCs. In conclusion, our data provide a new paradigm for Tif1 gamma in regulating the balance between lymphoid-and myeloid-derived HSCs through TGF-beta signaling, leading to HSC aging.

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