PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse

G.M. Tennant, Roger M. Wadsworth, Simon Kennedy

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Activation of PAR-2 in the vasculature affects vascular tone and adhesion of leukocytes to the endothelium. Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima formation, we hypothesised that mice lacking PAR-2 may have reduced neointima formation following vascular injury. PAR-2 activating peptides and trypsin induced endothelium-dependent relaxation of mouse carotid artery which was absent in the knockout mouse. Lack of a PAR-2 receptor did not affect lymphocyte adhesion under basal conditions, but reduced the contractile response produced by lymphocytes. Twenty-eight days after denuding injury, vessel contraction to lymphocytes was reduced in both strains while lymphocyte adhesion was significantly greater in PAR-2+/+ mice compared to the PAR-2 knockout mice. Neointimal area was markedly reduced in the PAR-2 knockout mouse. Our data show that PAR-2 modulates inflammatory cell adhesion when stimulated and in mice lacking the PAR-2 receptor, adhesion to injured vessels is reduced with a consequent reduction in neointima formation.
LanguageEnglish
Pages57-64
Number of pages7
JournalAtherosclerosis
Volume198
Issue number1
DOIs
Publication statusPublished - Sep 2007

Fingerprint

Neointima
Vascular System Injuries
Cell Adhesion
Knockout Mice
PAR-2 Receptor
Lymphocytes
Endothelium
Leukocytes
Carotid Arteries
Trypsin
Blood Vessels
Peptides
Wounds and Injuries

Keywords

  • protease activated receptor-2 (PAR-2)
  • lymphocyte
  • vascular injury
  • adhesion
  • neointima
  • pharmacology

Cite this

Tennant, G.M. ; Wadsworth, Roger M. ; Kennedy, Simon. / PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse. In: Atherosclerosis. 2007 ; Vol. 198, No. 1. pp. 57-64.
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PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse. / Tennant, G.M.; Wadsworth, Roger M.; Kennedy, Simon.

In: Atherosclerosis, Vol. 198, No. 1, 09.2007, p. 57-64.

Research output: Contribution to journalArticle

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AB - Activation of PAR-2 in the vasculature affects vascular tone and adhesion of leukocytes to the endothelium. Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima formation, we hypothesised that mice lacking PAR-2 may have reduced neointima formation following vascular injury. PAR-2 activating peptides and trypsin induced endothelium-dependent relaxation of mouse carotid artery which was absent in the knockout mouse. Lack of a PAR-2 receptor did not affect lymphocyte adhesion under basal conditions, but reduced the contractile response produced by lymphocytes. Twenty-eight days after denuding injury, vessel contraction to lymphocytes was reduced in both strains while lymphocyte adhesion was significantly greater in PAR-2+/+ mice compared to the PAR-2 knockout mice. Neointimal area was markedly reduced in the PAR-2 knockout mouse. Our data show that PAR-2 modulates inflammatory cell adhesion when stimulated and in mice lacking the PAR-2 receptor, adhesion to injured vessels is reduced with a consequent reduction in neointima formation.

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