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Chemokine stimulation of monocyte matrix metalloproteinase-9 requires endogenous TNF-alpha

Stephen C Robinson1, Kate A Scott, Frances R Balkwill

  • 1ICRF Translational Oncology Laboratory, Bart's and the London Queen Mary School of Dentistry, Charterhouse Square, London, EC1M 6BQ, GB. s.c.robinson@icrf.icnet.uk

Insights

Chemokines like CCL2 stimulate monocyte matrix metalloproteinase-9 (MMP-9) production via TNF-alpha, crucial for leukocyte extravasation in diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Leukocyte extravasation requires matrix-degrading enzymes, particularly matrix metalloproteinases (MMPs).
  • Monocyte production of MMPs is implicated in inflammatory diseases like cancer, asthma, and rheumatoid arthritis.

Purpose of the Study:

  • To investigate the role of CC chemokines in regulating MMP production in monocytes.
  • To elucidate the signaling pathways involved in chemokine-induced MMP release.

Main Methods:

  • Utilized THP-1 monocytic cells and peripheral blood monocytes (PBM).
  • Stimulated cells with CC chemokines (CCL2, CCL3, CCL5) and assessed MMP-9 protein and mRNA levels.
  • Investigated the role of autocrine TNF-alpha using neutralizing antibodies and an MMP inhibitor (BB 2516).

Main Results:

  • CC chemokines induced MMP-9 release in a bell-shaped dose-dependent manner.
  • MMP-9 production resulted from de novo synthesis, with increased mRNA levels preceding protein release.
  • Autocrine TNF-alpha was essential for chemokine-mediated MMP-9 induction, as confirmed by antibody neutralization and MMP inhibitor studies.

Conclusions:

  • Chemokines regulate monocyte MMP-9 production through an autocrine TNF-alpha-dependent pathway.
  • Understanding these mechanisms may offer novel therapeutic targets for diseases involving leukocyte extravasation.

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