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Cited by 447Hematopoietic Stem Cell TransplantationMesenchymal stem cell researchBlood disorders and treatments

Cell cycle regulation in hematopoietic stem cells

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Pietras, Eric M., Warr, Matthew R., Passegué, Emmanuelle·2011·Journal of Cell Biology
DOI 10.1083/jcb.201102131PMC PMC3257565
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Abstract

Hematopoietic stem cells (HSCs) give rise to all lineages of blood cells. Because HSCs must persist for a lifetime, the balance between their proliferation and quiescence is carefully regulated to ensure blood homeostasis while limiting cellular damage. Cell cycle regulation therefore plays a critical role in controlling HSC function during both fetal life and in the adult. The cell cycle activity of HSCs is carefully modulated by a complex interplay between cell-intrinsic mechanisms and cell-extrinsic factors produced by the microenvironment. This fine-tuned regulatory network may become altered with age, leading to aberrant HSC cell cycle regulation, degraded HSC function, and hematological malignancy.

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  • Activation of mitogenic pathways such as PI3K-AKT by inflammatory signals induces post-translational modifications of cell cycle regulatory proteins to potentiate cell cycle progression.

    “it is well known that the activation of mitogenic pathways such as PI3K-AKT by inflammatory signals induces the necessary post-translational modifications (e.g., phosphorylation) of cell cycle regulatory proteins to potentiate cell cycle progression (Chang et al., 2003; Pietras et al., 2011; Warr et al., 2011; Pietras et al., 2014).”

    From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Pietras et al., 2011

    The PI3K signaling pathway section says PI3K/Akt promotes HSC proliferation, and the cell-extrinsic mechanisms section suggests inflammatory interferons may induce HSC cell-cycle entry partly through Akt. The Rb Family section describes phosphorylation of cell-cycle regulators during progression, but the paper does not establish that inflammatory activation of PI3K-Akt induces those post-translational modifications; its interferon–Akt link is also hedged. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Pietras, E. M., Warr, M. R., & Passegué, E.
Affiliations
  • University of California, San Francisco (US)
  • Department of Medicine, Division of Hematology/Oncology, The Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA 94143
ORCID
Venue
Journal of Cell Biology
Publisher
Rockefeller University Press
Published
2011-11-28
Volume
195
Issue
5
Pages
709-720
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
DOI
10.1083/jcb.201102131
PMC
PMC3257565
OpenAlex
W2121709505
Cited by
447
References
18
Citations by year
2026: 9 · 2025: 21 · 2024: 22 · 2023: 21 · 2022: 22 · 2021: 29 · 2020: 34 · 2019: 32 · 2018: 41 · 2017: 30 · 2016: 34 · 2015: 39 · 2014: 39 · 2013: 40 · 2012: 9
FWCI
3.90
Type
journal article
Language
en
Open access
Locations
  • The Journal of Cell Biology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL092471)
Topics
  • Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
Keywords
hematopoietic stem cells, cell cycle regulation, stem cell quiescence, stem cell proliferation, blood homeostasis, aging, hematologic malignancies, fetal hematopoiesis
MeSH terms
Aging, Animals, Cell Cycle, Embryo, Mammalian, Hematopoietic Stem Cells, Models, Biological, Signal Transduction, Cell Cycle Proteins, Cell Proliferation, Mice

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