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Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
06:46

Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages

Published on: June 30, 2016

Colony-stimulating factor-1 (CSF-1) delivers a proatherogenic signal to human macrophages

Katharine M Irvine1, Melanie R Andrews, Manuel A Fernandez-Rojo

  • 1The University of Queensland, Institute for Molecular Bioscience, Brisbane, Queensland, Australia.

Journal of Leukocyte Biology
|November 14, 2008
PubMed

Insights

Colony-stimulating factor 1 (CSF-1) promotes a proatherogenic environment in human macrophages by altering gene expression and cholesterol metabolism. This suggests CSF-1 contributes to cardiovascular disease progression.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Colony-stimulating factor 1 (CSF-1) is known to influence monocyte and macrophage functions.
  • While CSF-1's role in mouse macrophages is established, its acute effects on human macrophages are less understood.
  • CSF-1 is implicated in inflammation and is found in atherosclerotic lesions.

Purpose of the Study:

  • To investigate the acute effects of CSF-1 on mature human monocyte-derived macrophages (HMDM).
  • To determine how CSF-1 modulates the HMDM transcriptome and influences pathways related to atherosclerosis.
  • To explore the potential mechanisms by which CSF-1 contributes to cardiovascular disease.

Main Methods:

  • Human monocyte-derived macrophages (HMDM) were treated with CSF-1.
  • Gene expression profiling was used to analyze transcriptome changes.
  • Levels of specific chemokines, cholesterol transporters, and cholesterol biosynthesis enzymes were assessed.
  • Cellular free cholesterol levels were measured.
  • The effect of a selective CSF-1 receptor kinase inhibitor (GW2580) was evaluated.

Main Results:

  • CSF-1 did not induce urokinase plasminogen activator mRNA or repress apolipoprotein E mRNA in HMDM, unlike in mouse macrophages.
  • CSF-1 did not prime LPS-induced TNF and IL-6 secretion.
  • CSF-1 modulated the HMDM transcriptome, favoring a proatherogenic environment.
  • CSF-1 induced proatherogenic chemokines (CXCL10, CCL2, CCL7) and repressed the antiatherogenic CXCR4.
  • CSF-1 upregulated cholesterol biosynthesis genes and repressed the cholesterol efflux transporter ABCG1.
  • CSF-1 increased free cholesterol levels in HMDM, an effect blocked by GW2580.

Conclusions:

  • CSF-1 promotes a proatherogenic environment in human macrophages.
  • CSF-1 influences macrophage cholesterol metabolism, increasing free cholesterol levels.
  • These findings link CSF-1 to inflammation and cardiovascular disease, suggesting roles in atherosclerotic plaque progression.

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