scholarly journals Cell-Cycle-Specific Function of p53 in Fanconi Anemia Hematopoietic Stem and Progenitor Cell Proliferation

2018 ◽  
Vol 10 (2) ◽  
pp. 339-346 ◽  
Author(s):  
Xiaoli Li ◽  
Andrew F. Wilson ◽  
Wei Du ◽  
Qishen Pang
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Fanconi Anemia ◽  
Progenitor Cell ◽  
Specific Function ◽  
Hematopoietic Stem ◽  
Progenitor Cell Proliferation

scholarly journals Histone chaperone HIRA regulates neural progenitor cell proliferation and neurogenesis via β-catenin

2017 ◽  
Vol 216 (7) ◽  
pp. 1975-1992 ◽  
Author(s):  
Yanxin Li ◽  
Jianwei Jiao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Progenitor Cell ◽  
Neural Progenitor Cells ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Histone Chaperone ◽  
Epigenetic Mechanism ◽  
Progenitor Cell Proliferation ◽  
Early Neurogenesis

Histone cell cycle regulator (HIRA) is a histone chaperone and has been identified as an epigenetic regulator. Subsequent studies have provided evidence that HIRA plays key roles in embryonic development, but its function during early neurogenesis remains unknown. Here, we demonstrate that HIRA is enriched in neural progenitor cells, and HIRA knockdown reduces neural progenitor cell proliferation, increases terminal mitosis and cell cycle exit, and ultimately results in premature neuronal differentiation. Additionally, we demonstrate that HIRA enhances β-catenin expression by recruiting H3K4 trimethyltransferase Setd1A, which increases H3K4me3 levels and heightens the promoter activity of β-catenin. Significantly, overexpression of HIRA, HIRA N-terminal domain, or β-catenin can override neurogenesis abnormities caused by HIRA defects. Collectively, these data implicate that HIRA, cooperating with Setd1A, modulates β-catenin expression and then regulates neurogenesis. This finding represents a novel epigenetic mechanism underlying the histone code and has profound and lasting implications for diseases and neurobiology.

scholarly journals DEK Regulates Hematopoietic Stem Engraftment and Progenitor Cell Proliferation

2012 ◽  
Vol 21 (9) ◽  
pp. 1449-1454 ◽  
Author(s):  
Hal E. Broxmeyer ◽  
Ferdinand Kappes ◽  
Nirit Mor-Vaknin ◽  
Maureen Legendre ◽  
John Kinzfogl ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Hematopoietic Stem ◽  
Progenitor Cell Proliferation

Transforming growth factor β1 mediates cell-cycle arrest of primitive hematopoietic cells independent of p21Cip1/Waf1or p27Kip1

Blood ◽  
2001 ◽  
Vol 98 (13) ◽  
pp. 3643-3649 ◽  
Author(s):  
Tao Cheng ◽  
Hongmei Shen ◽  
Neil Rodrigues ◽  
Sebastian Stier ◽  
David T. Scadden
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Progenitor Cell ◽  
Transforming Growth Factor ◽  
Hematopoietic Cells ◽  
Transforming Growth Factor Β1 ◽  
Primitive Cell ◽  
Hematopoietic Stem ◽  
Tgf Β1

Abstract The regulation of stem cell proliferation is a poorly understood process balancing rapid, massive blood cell production in times of stress with maintenance of a multipotent stem cell pool over decades of life. Transforming growth factor β1 (TGF-β1) has pleiotropic effects on hematopoietic cells, including the inhibition of primitive cell proliferation. It was recently demonstrated that the cyclin-dependent kinase inhibitors, p21Cip1/Waf1 (p21) and p27Kip1 (p27), can inhibit the proliferation of hematopoietic stem cells and progenitor cells, respectively. The relation of TGF-β1 stimulation to p21 and p27 was examined using a fine-mapping approach to gene expression in individual cells. Abundant TGF-β1 expression and p21 expression were documented in quiescent, cytokine-resistant hematopoietic stem cells and in terminally differentiated mature blood cells, but not in proliferating progenitor cell populations. TGF-β1 receptor (TβR II) was expressed ubiquitously without apparent modulation. Cell- cycle–synchronized 32D cells exposed to TGF-β1 demonstrated a marked antiproliferative effect of TGF-β1, yet neither the level of p21 mRNA nor the protein level of either p21 or p27 was altered. To corroborate these observations in primary cells, bone marrow mononuclear cells derived from mice engineered to be deficient in p21 or p27 were assessed. Progenitor and primitive cell function was inhibited by TGF-β1 equivalently in −/− and +/+ littermate controls. These data indicate that TGF-β1 exerts its inhibition on cell cycling independent of p21 and p27 in hematopoietic cells. TGF-β1 and p21 or p27 participate in independent pathways of stem cell regulation, suggesting that targeting each may provide complementary strategies for enhancing stem or progenitor cell expansion and gene transduction.

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