Essential role for proteinase-activated receptor-2 in arthritis
J. Clin. Invest. William R. Ferrell, et al. 111:35 doi:10.1172/JCI16913 [
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Figure 3Effects of PAR-2 agonists on synovial perfusion and joint swelling. (
a) Laser Doppler image showing vasodilatation 1 minute after topical administration of 1 μg of the PAR-2 agonist SLIGRL-NH
2 (SLIG) to
PAR-2+/+ mice. (
b) ASKH95 (1 μg) administered to
PAR-2+/+ mice also elicits vasodilatation. (
c) ASKH95 (1 μg) administered to
PAR-2–/– mice is without effect. (
d) The control peptide ASKH115 (1 μg) administered to
PAR-2+/+ mice is without effect. (
e) Histogram showing quantitative data for the vasodilator effect of SLIG in
PAR-2+/+ mice (+/+ SLIG), ASKH95 in both
PAR-2–/– mice (–/– 95) and wild-type mice (+/+ 95), and ASKH115 in wild-type mice (+/+ 115). Perfusion is measured in arbitrary “flux units” and color coded in the images, with dark blue being the lowest and dark red the highest. Data are presented as mean ± SEM.
n = 5–7. *
P < 0.01 compared with +/+ 95. (
f) Intra-articular injection of 100 μg of SLIG in
PAR-2+/+ mice (filled squares) elicits an increase in joint diameter that reaches a maximum within 4 hours but declines thereafter. The synthetic PAR-2 agonist ASKH95 (100 μg) produces joint swelling that reaches maximum by 24 hours and is sustained thereafter in
PAR-2+/+ mice (filled circles), a response that differs significantly compared with the same dose of this peptide in
PAR-2–/– mice (open circles) and control peptide ASKH115 in wild-type mice (filled triangles). Data are presented as mean ± SEM;
n = 4–10.
