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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
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Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
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Hematopoiesis, or blood cell production, is a vital biological process that begins early in embryonic development and continues throughout life. This process generates the various types of cells found in blood, including red blood cells, white blood cells, and platelets from hematopoietic stem cells (HSCs).
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Hemangioblasts are multipotent stem cells originating from the mesoderm. They give rise to hematopoietic stem cells (HSCs), which undergo hematopoiesis to produce all the formed elements of blood. This process is regulated by a complex network of hematopoietic growth factors, including transcription factors, growth factors, and cytokines. These factors stimulate the HSCs to divide and differentiate, though some HSCs remain undifferentiated to maintain a self-renewing pool.
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The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...
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MAFB regulates hematopoietic stem cell proliferation and maintenance.

Saki Asano1, Ching-Wei Liao1,2, Yurina Matsunaga1

  • 1Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

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Summary

MAFB plays distinct roles in fetal and adult hematopoietic stem cells (HSCs). Deleting MAFB boosts fetal HSC proliferation but impairs adult HSC maintenance, impacting long-term repopulation.

Keywords:
Cell cycle regulationHematopoietic stem cells (HSCs)MAFBSelf-renewalStem cell exhaustion

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Area of Science:

  • Hematology
  • Developmental Biology
  • Stem Cell Biology

Background:

  • The transcription factor MAFB (large Maf family) is present in fetal liver (FL) and bone marrow (BM) hematopoietic stem cells (HSCs).
  • The specific functions of MAFB in HSCs across different developmental stages are not well understood.

Purpose of the Study:

  • To investigate the distinct roles of MAFB in FL and BM HSCs.
  • To elucidate MAFB's stage-dependent regulation of HSC function, including proliferation and long-term maintenance.

Main Methods:

  • Utilized Mafb-deficient and Mafb-GFP knock-in mouse models.
  • Performed transplantation assays (including serial transplantation) and colony-forming capacity assays.
  • Analyzed long-term HSC (LT-HSC) populations and multilineage differentiation potential in Mafb conditional knockout (cKO) mice.

Main Results:

  • Mafb deletion in FL HSCs enhanced proliferation, cell cycle entry, and myeloid differentiation, improving chimerism.
  • Mafb deficiency in BM HSCs resulted in impaired long-term reconstitution and progressive exhaustion.
  • Mafb cKO in adult HSCs led to a significant reduction in LT-HSCs and their differentiation potential.

Conclusions:

  • MAFB acts as a stage-dependent regulator, promoting HSC proliferation during fetal development.
  • MAFB is crucial for maintaining HSC function and long-term repopulation capacity in adult life.
  • Findings highlight MAFB's role in HSC cell cycle control and its implications for understanding HSC regulation across life stages.