C-reactive protein induces M-CSF release and macrophage proliferation

Sridevi Devaraj, Jung Mi Yun, Catherine Duncan-Staley, Ishwarlal Jialal

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Inflammation is pivotal in atherosclerosis. M-CSF regulates macrophage growth and differentiation and plays a role in atherogenesis. C-reactive protein (CRP), a cardiovascular risk marker, may promote atherogenesis. However, the effects of CRP on M-CSF release and subsequent macrophage proliferation have not been examined previously. Human aortic endothelial cells (HAEC) were incubated with boiled CRP or native CRP 12.5, 25, and 50 μg/mL for 12-15 h, and M-CSF release was examined by flow cytometry and ELISA. CRP resulted in a significant and dose-dependent increase in M-CSF mRNA and secretion from HAEC as well as human monocyte-derived macrophages (HMDM; P<0.01). Furthermore, conditioned medium (5%) from HAEC pretreated with CRP, when incubated with HMDM, increased macrophage proliferation significantly. This was blocked with M-CSF antibody but not irrelevant antibody. Inhibition of NF-κB resulted in significant abrogation of CRP-induced M-CSF release and subsequent macrophage proliferation. Antibodies to CD32 and CD64 but not CD16 abrogated CRP-induced M-CSF release. Thus, CRP upregulates M-CSF release from HMDM and HAEC and increased macrophage proliferation. These effects appear to be mediated via activation of NF-κB via CD32 and CD64. These studies provide further evidence for a proatherogenic role for CRP.

Original languageEnglish (US)
Pages (from-to)262-267
Number of pages6
JournalJournal of Leukocyte Biology
Volume85
Issue number2
DOIs
StatePublished - Feb 1 2009

Keywords

  • CRP
  • Inflammation
  • Mechanistic insights

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

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