Novel antagonists for proteinase-activated receptor 2: inhibition of cellular and vascular responses in vitro and in vivo

Br J Pharmacol. 2009 Sep;158(1):361-71. doi: 10.1111/j.1476-5381.2009.00342.x.

Abstract

Background and purpose: Proteinase-activated receptor 2 (PAR(2)) is a G-protein coupled receptor associated with many pathophysiological functions. To date, the development of PAR(2) antagonists has been limited. Here, we identify a number of novel peptide-mimetic PAR(2) antagonists and demonstrate inhibitory effects on PAR(2)-mediated intracellular signalling pathways and vascular responses.

Experimental approach: The peptide-mimetic compound library based on the structures of PAR(2) agonist peptides were screened for inhibition of PAR(2)-induced calcium mobilisation in human keratinocytes. Representative compounds were further evaluated by radioligand binding and inhibition of NFkappaB transcriptional activity and IL-8 production. The vascular effects of the antagonists were assessed using in vitro and in vivo models.

Key results: Two compounds, K-12940 and K-14585, significantly reduced SLIGKV-induced Ca(2+) mobilisation in primary human keratinocytes. Both K-12940 and K-14585 exhibited competitive inhibition for the binding of a high-affinity radiolabelled PAR(2)-ligand, [(3)H]-2-furoyl-LIGRL-NH(2), to human PAR(2) with K(i) values of 1.94 and 0.627 microM respectively. NFkappaB reporter activity and IL-8 production were also significantly reduced. Furthermore, relaxation of rat-isolated aorta induced by SLIGRL-NH(2) was inhibited competitively by K-14585. K-14585 also significantly lowered plasma extravasation in the dorsal skin of guinea pigs and reduced salivation in mice.

Conclusions and implications: K-12940 and K-14585 antagonized PAR(2) competitively, resulting in inhibition of PAR(2)-mediated signalling and physiological responses both in vitro and in vivo. These peptide-mimetic PAR(2) antagonists could be useful in evaluating PAR(2)-mediated biological events and might lead to a new generation of therapeutically useful antagonists.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta, Thoracic / drug effects
  • Aorta, Thoracic / physiology
  • Binding, Competitive / drug effects
  • Binding, Competitive / physiology
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology
  • Capillary Permeability / drug effects
  • Capillary Permeability / physiology*
  • Cell Line
  • Cells, Cultured
  • Guinea Pigs
  • Humans
  • In Vitro Techniques
  • Keratinocytes / drug effects
  • Keratinocytes / enzymology
  • Keratinocytes / physiology*
  • Male
  • Mice
  • Molecular Mimicry
  • Oligopeptides / pharmacology*
  • Peptides / agonists
  • Peptides / antagonists & inhibitors*
  • Peptides / physiology*
  • Rats
  • Rats, Wistar
  • Receptor, PAR-2 / agonists
  • Receptor, PAR-2 / antagonists & inhibitors*
  • Receptor, PAR-2 / physiology*
  • Urea / analogs & derivatives*
  • Urea / pharmacology

Substances

  • K 12940
  • K-14585
  • Oligopeptides
  • Peptides
  • Receptor, PAR-2
  • Urea