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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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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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Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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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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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Splenic fibroblasts control marginal zone B cell movement and function via two distinct Notch2-dependent regulatory

Anneka Allman1, Brian T Gaudette2, Samantha Kelly1

  • 1Division of Hematology/Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Immunity
|December 28, 2024
PubMed
Summary

Splenic marginal zone B cells require Delta-like1 (Dll1) Notch ligands for proper function. This signaling regulates cell growth and migration, crucial for immune response to microbes.

Keywords:
B cellsNotchchemotaxisfibroblastic reticular cellsmarginal zonespleen

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Area of Science:

  • Immunology
  • Cell Biology
  • Developmental Biology

Background:

  • Innate-like splenic marginal zone (MZ) B (MZB) cells are critical for rapid responses to blood-borne pathogens.
  • The mechanisms integrating extrinsic and intrinsic factors for accelerated MZB cell responsiveness remain largely unknown.

Purpose of the Study:

  • To investigate the role of Delta-like1 (Dll1) Notch ligands in regulating MZB cell biology.
  • To elucidate the downstream signaling pathways involved in MZB cell programming.

Main Methods:

  • Utilized genetic manipulation in mice to study Dll1 function.
  • Analyzed gene expression related to cell growth and migration.
  • Investigated the role of sphingosine-1 phosphate receptor 1 (S1PR1) in B cell localization.

Main Results:

  • Dll1, but not Dll4, ligands from splenic fibroblasts are essential for MZB cell pool size, migration, and function.
  • D111-Notch2 signaling controls both Myc-dependent cell growth and Myc-independent regulation of cell movement, including S1PR1.
  • S1pr1 deficiency impairs MZB cell entry into the MZ and leads to splenic retention upon Notch signaling withdrawal.

Conclusions:

  • Specialized splenic niches, via Dll1-Notch2 signaling, program MZB cells for a poised state and patrolling behavior.
  • Conserved Myc-dependent and Myc-independent Notch2-regulated mechanisms are key to MZB cell function.
  • These findings have implications for understanding human B cell subsets and lymphomas.