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Adherence-dependent increase in human monocyte PDGF(B) mRNA is associated with increases in c-fos, c-jun, and EGR2

R J Shaw1, D E Doherty, A G Ritter

  • 1Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.

Insights

Monocyte adherence triggers gene activation, increasing platelet-derived growth factor B subunit (PDGF(B)) mRNA. This process involves cytoskeletal changes and early growth response genes, influencing cell priming.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Monocyte to macrophage differentiation is crucial for tissue repair and immune response.
  • This transition involves changes in gene expression and growth factor production.
  • Adherence to surfaces is a key initial step in monocyte differentiation.

Purpose of the Study:

  • To investigate if monocyte adherence triggers gene activation for profibrotic growth factors.
  • To determine the role of cytoskeletal integrity in adherence-induced gene expression.
  • To explore the relationship between adherence, early growth response genes, and PDGF(B) mRNA levels.

Main Methods:

  • In vitro adherence of human monocytes to coated plastic surfaces.
  • Quantification of mRNA levels for PDGF(B), TGF-beta, c-fos, c-jun, and EGR2 using techniques like RT-PCR.
  • Pharmacological disruption of cytoskeletal integrity using cytochalasin D.

Main Results:

  • Monocyte adherence induced a biphasic increase in PDGF(B) mRNA, with peaks at 6 hours and 13 days.
  • The 6-hour PDGF(B) mRNA increase was adherence-dependent and abrogated by cytochalasin D.
  • Adherence led to increased mRNA for c-fos, c-jun, and EGR2, with c-jun and EGR2 increases also dependent on cytoskeletal integrity.

Conclusions:

  • Monocyte adherence is a significant trigger for the upregulation of specific genes, including PDGF(B).
  • Cytoskeletal rearrangement plays a critical role in the adherence-induced expression of c-jun, EGR2, and PDGF(B) mRNA.
  • These findings suggest a mechanism for differential cell priming during monocyte differentiation.

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