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CD47 expression is decreased in hematopoietic progenitor cells in patients with myelofibrosis

A Nonino1,2, J M Nascimento2,3, C C Mascarenhas1

  • 1Programa de Pós-Graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília, Brasília, DF, Brasil.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|December 13, 2018
PubMed

Insights

Myelofibrosis (MF) involves abnormal blood stem cells. Researchers found CD47 protein levels were unexpectedly lower in MF progenitor cells compared to healthy individuals.

Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Myelofibrosis (MF) is a bone marrow disorder characterized by fibrosis, abnormal cytokine levels, and increased circulating hematopoietic progenitor cells (HPCs).
  • CD47 is a cell surface protein that inhibits phagocytosis and is often upregulated in cancer stem cells and mobilized normal stem cells.
  • The role of CD47 in MF, particularly in relation to progenitor cells, is not well understood.

Purpose of the Study:

  • To investigate and compare CD47 expression levels in hematopoietic progenitor cells (HPCs) between patients with myelofibrosis (MF) and healthy controls.
  • To determine if cytokines implicated in MF pathogenesis, such as transforming growth factor β (TGF-β) and stromal-derived factor 1 (SDF-1), influence CD47 expression on normal HPCs.

Main Methods:

  • Flow cytometry was used to quantify CD47 expression on HPCs isolated from MF patients and healthy donors.
  • Control HPCs were cultured with TGF-β and SDF-1 to assess the impact of these cytokines on CD47 expression.

Main Results:

  • CD47 expression was found to be significantly decreased on hematopoietic progenitor cells (HPCs) from patients with myelofibrosis (MF) compared to healthy controls.
  • Exposure of normal HPCs to TGF-β and SDF-1 did not alter CD47 expression levels.

Conclusions:

  • The decreased expression of CD47 on MF progenitor cells suggests a potential role in the disease pathophysiology, contrary to its typical upregulation in other cancers.
  • These findings indicate that the dysregulation of CD47 in MF is not directly mediated by the overexpressed cytokines TGF-β and SDF-1.

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