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EMMPRIN (CD147) regulation of MMP-9 in bronchial epithelial cells in COPD

Stephane Jouneau1, Nadia Khorasani, Patricia DE Souza

  • 1Experimental Studies, Airway Disease Section, National Heart and Lung Institute, Imperial College London Royal Brompton Hospital, London, UK.

Respirology (Carlton, Vic.)
|March 2, 2011
PubMed
Abstract

Insights

Extracellular matrix metalloproteinase inducer (EMMPRIN) is elevated in COPD patients, primarily released by bronchial epithelial cells. EMMPRIN drives matrix metalloproteinase-9 (MMP-9) production, a key factor in COPD pathogenesis.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Cell Biology

Background:

  • Chronic Obstructive Pulmonary Disease (COPD) is characterized by inflammation and tissue remodeling.
  • Matrix metalloproteinases (MMPs), particularly MMP-9, are implicated in COPD pathogenesis.
  • Extracellular matrix metalloproteinase inducer (EMMPRIN, also known as CD147) is a known inducer of MMP production.

Purpose of the Study:

  • To investigate the cellular origin of EMMPRIN in COPD.
  • To determine the role of EMMPRIN in MMP-9 production in COPD patients.

Main Methods:

  • Bronchial biopsies, macrophages (AM, BM), and epithelial cells (EC) from COPD patients and controls were analyzed.
  • EMMPRIN levels were quantified in various biological samples and tissues.
  • MMP-9 activity and mRNA expression were measured following EMMPRIN blockade.

Main Results:

  • EMMPRIN levels and expression were significantly higher in COPD patients, particularly in bronchial epithelial cells.
  • Bronchial epithelial cells secreted more EMMPRIN than macrophages.
  • Blocking EMMPRIN reduced MMP-9 activity and mRNA in epithelial cells, but not in macrophages.

Conclusions:

  • Bronchial epithelial cells are a major source of increased EMMPRIN in COPD.
  • EMMPRIN plays a significant role in regulating MMP-9 expression in COPD.

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