The FLT3 Tyrosine Kinase Receptor Inhibits Neural Stem/Progenitor Cell Proliferation and Collaborates with NGF to Promote Neuronal Survival

2001 ◽  
Vol 18 (4) ◽  
pp. 381-393 ◽  
Author(s):  
Christine Y. Brazel ◽  
Melissa H. Ducceschi ◽  
Bronislaw Pytowski ◽  
Steven W. Levison
Keyword(s):  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Progenitor Cell ◽  
Neuronal Survival ◽  
Tyrosine Kinase Receptor ◽  
Progenitor Cell Proliferation

scholarly journals Mobilization of CD34+ Progenitor Cells in Association with Decreased Proliferation in the Bone Marrow of Macaques after Administration of the Fms-Like Tyrosine Kinase 3 Ligand

2010 ◽  
Vol 17 (8) ◽  
pp. 1269-1273 ◽  
Author(s):  
R. Keith Reeves ◽  
Qing Wei ◽  
Patricia N. Fultz
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Flow Cytometric ◽  
Progenitor Cell Proliferation ◽  
Cell Mobilization ◽  
Negative Regulatory Mechanism

ABSTRACT Fms-like tyrosine kinase 3 ligand (FLT3-L) is critical for the differentiation and self-renewal of CD34+ progenitor cells in primates and has been used therapeutically to mobilize progenitor and dendritic cells in vivo. However, little is known regarding the expansion of progenitor cells outside of peripheral blood, particularly in bone marrow (BM), where progenitor cells primarily reside. Evaluation of FLT3-L-mediated cell mobilization during lentivirus infections, where the numbers of CD34+ progenitor cells are reduced, is limited. We enumerated frequencies and absolute numbers of CD34+ progenitor cells in blood and BM of naive and SIV- or SHIV-infected macaques during and after the administration of FLT3-L. Flow cytometric analyses revealed that, while CD34+ cells increased in the circulation, no expansion was observed in BM. Furthermore, in the BM intracellular Ki67, a marker of cell proliferation, was downregulated in CD34+ progenitor cells but was upregulated significantly in the bulk cell population. Although the exact mechanism(s) remains unclear, these data suggest that CD34+ cell mobilization in blood was the result of cellular emigration from BM and not the proliferation of CD34+ cells already in the periphery. It is possible that the decreased progenitor cell proliferation observed in BM is evidence of a negative regulatory mechanism preventing hyperproliferation and development of neoplastic cells.

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 The cell biology of regeneration

2012 ◽  
Vol 196 (5) ◽  
pp. 553-562 ◽  
Author(s):  
Ryan S. King ◽  
Phillip A. Newmark
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Biology ◽  
Progenitor Cell ◽  
Complex Structures ◽  
Regenerative Processes ◽  
Cellular Behavior ◽  
Positional Identity ◽  
Progenitor Cell Proliferation ◽  
Functional Analyses

Regeneration of complex structures after injury requires dramatic changes in cellular behavior. Regenerating tissues initiate a program that includes diverse processes such as wound healing, cell death, dedifferentiation, and stem (or progenitor) cell proliferation; furthermore, newly regenerated tissues must integrate polarity and positional identity cues with preexisting body structures. Gene knockdown approaches and transgenesis-based lineage and functional analyses have been instrumental in deciphering various aspects of regenerative processes in diverse animal models for studying regeneration.

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