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Splenic hematopoietic stem cells display a pre-activated phenotype.

Emilie Coppin1, Jonathan Florentin1, Sathish Babu Vasamsetti1

  • 1Division of Cardiology, Department of Medicine, Vascular Medicine Institute, University of Pittsburgh Medical Center, BST 1720.1, 200 Lothrop Street, Pittsburgh, PA, 15213, USA.

Immunology and Cell Biology
|March 12, 2018
PubMed
Summary

Splenic hematopoietic stem cells (HSCs) are pre-activated, unlike bone marrow HSCs. This splenic HSC state, influenced by the microenvironment and Mtg16, allows faster cell cycle entry during emergencies like septic shock.

Keywords:
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Area of Science:

  • Hematopoiesis research
  • Stem cell biology
  • Immunology

Background:

  • Splenic hematopoiesis is vital for diseases like myocardial infarction and atherosclerosis.
  • The spleen stores myeloid cells for rapid release during inflammation.
  • The cellular and molecular mechanisms of splenic hematopoiesis are not well understood.

Purpose of the Study:

  • To investigate the cell cycle status and regulation of splenic hematopoietic stem cells (HSCs).
  • To compare splenic HSCs with bone marrow HSCs in terms of cell cycle and environmental influences.
  • To identify molecular factors regulating splenic HSC cell cycle.

Main Methods:

  • Comparative analysis of hematopoietic stem cell (HSC) cell cycle phases in spleen versus bone marrow.
  • Gene expression profiling of splenic and bone marrow HSCs.
  • Mobilization and transplantation experiments.
  • Analysis of Mtg16 (myeloid translocation gene 16) deficiency effects on HSCs.

Main Results:

  • Most splenic HSCs are in the G1 phase, indicating a pre-activated state, unlike bone marrow HSCs.
  • Splenic HSCs show enrichment in G0-G1 transition genes and lower G1-S transition gene expression.
  • Splenic HSCs rapidly enter S-G2-M phases during septic shock, while bone marrow HSCs do not.
  • Bone marrow HSCs adopt a pre-activated splenic HSC cell cycle status upon transplantation into the spleen.
  • Mtg16 deficiency accelerates splenic HSC entry into S-G2-M phases, but not bone marrow HSCs.

Conclusions:

  • Splenic HSCs are intrinsically pre-activated compared to bone marrow HSCs.
  • The splenic microenvironment plays a key role in pre-activating splenic HSCs.
  • Mtg16 acts as an intrinsic negative regulator of G1-S transition in splenic HSCs.
  • This pre-activated state of splenic HSCs facilitates rapid responses in emergency conditions.