A protease activated receptor-2 (PAR-2) activating peptide, tc-LIGRLO-NH2, induces protease release from mast cells: role in TNF degradation

BMC Pharmacol. 2004 Jul 20:4:12. doi: 10.1186/1471-2210-4-12.

Abstract

Background: Mast cell (MC)-derived serine proteases have been implicated in a variety of inflammatory processes. We have previously shown that rat peritoneal MC (PMC) express mRNA for protease activated receptor 2 (PAR-2), a G-coupled receptor activated by trypsin-like proteases. Recent evidence also suggests that MC-induced inflammation can be mediated through PAR. Therefore, we hypothesized that specific PAR-2 agonist peptides (PAR-2ap) induce protease release from PMC.

Results: Western blot analysis of PMC supernatants revealed that a PAR-2ap, tc-LIGRLO (10 microM), stimulated the release of rat MC protease (RMCP)-1, RMCP-5 and carboxypeptidase-A. The release was evident by 20 min but further increased up to 8 h. To study the biological effects of protease release we tested supernatants from tc-LIGRLO, tc-OLRGIL (inactive control peptide) and antigen-activated PMC for proteolytic activity by seeding with TNF (150 pg/ml), incubating for 8 h at 37 degrees C, and measuring TNF remaining in the supernatants. Supernatants from tc-LIGRLO-stimulated PMC degraded 44 % of seeded TNF (n = 5). Moreover, this TNF proteolysis was dependent on the concentration of tc-LIGRLO used to stimulate PMC, and was significantly inhibited (94 %) by soybean trypsin inhibitor. Antigen and tc-OLRGIL induced no significant release of such proteolytic activity.

Conclusions: These data indicate that a PAR-2ap induces the release of proteases from mast cells, which may degrade extracellular cytokines and other substrates thus modulating the inflammatory response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carboxypeptidases A / metabolism
  • Chymases
  • In Vitro Techniques
  • Inflammation / metabolism
  • Male
  • Mast Cells / drug effects
  • Mast Cells / enzymology*
  • Oligopeptides / pharmacology*
  • Peptide Hydrolases / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, PAR-2 / drug effects
  • Receptor, PAR-2 / metabolism*
  • Receptor, PAR-2 / physiology
  • Serine Endopeptidases / metabolism
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • 2-furoyl-LIGRLO-amide
  • Oligopeptides
  • Receptor, PAR-2
  • Tumor Necrosis Factor-alpha
  • Peptide Hydrolases
  • Carboxypeptidases A
  • Serine Endopeptidases
  • Chymases