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Protease-activated receptor-2 (PAR-2) is a weak enhancer of mucin secretion by human bronchial epithelial cells in

Ko-Wei Lin1, Joungjoa Park, Anne L Crews

  • 1Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA.

The International Journal of Biochemistry & Cell Biology
|December 14, 2007
PubMed

Insights

Protease-activated receptor-2 (PAR-2) activation showed a minor effect on mucin secretion in airway epithelial cells. This suggests PAR-2 is unlikely to be a major factor in mucus overproduction during airway inflammation.

Area of Science:

  • Cell Biology
  • Respiratory Medicine
  • G-protein-coupled receptors

Background:

  • Protease-activated receptor-2 (PAR-2) is a G-protein-coupled receptor activated by serine proteases.
  • PAR-2 expression increases in respiratory epithelium during asthma and COPD, conditions marked by excessive mucus production.

Purpose of the Study:

  • To investigate the potential link between PAR-2 activation and mucin hypersecretion in airway epithelial cells.
  • To determine if PAR-2 plays a significant role in the excessive mucus production observed in inflammatory airway diseases.

Main Methods:

  • Utilized normal human bronchial epithelial (NHBE) cells and human bronchial epithelial cell lines (NCI-H292, HBE-1).
  • Exposed cells to a synthetic PAR-2 agonist peptide (SLIGKV-NH2) and measured mucin secretion.
  • Assessed the effect of known PAR-2 agonists (trypsin, tryptase) and employed siRNA for PAR-2 knockdown.

Main Results:

  • NHBE, NCI-H292, and HBE-1 cells expressed significant levels of PAR-2 protein.
  • A synthetic PAR-2 agonist peptide caused a small, concentration-dependent increase in mucin secretion at high doses.
  • Neither human lung tryptase nor bovine pancreatic trypsin affected mucin secretion; PAR-2 knockdown abolished the peptide agonist's effect.

Conclusions:

  • PAR-2 activation results in only a weak stimulation of mucin secretion by human airway epithelial cells in vitro.
  • PAR-2 is unlikely to be a significant contributor to the mucin hypersecretion characteristic of inflamed airways in conditions like asthma and COPD.

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