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Kinin B1 receptor regulates inflammatory cell recruitment during low laminar shear stress
Author(s) -
Martin Katherine,
Perretti Mauro,
Ahluwalia Amrita
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.646.4
Subject(s) - kinin , receptor , cytokine , inflammation , receptor antagonist , microbiology and biotechnology , cell , endothelial stem cell , immunology , chemistry , biology , endocrinology , in vitro , medicine , antagonist , bradykinin , biochemistry
The kinin B1 receptor (B1R) is an inducible receptor that is only weakly expressed, if at all, under normal physiological conditions but is induced under situations of stress. We have previously shown that when endothelial cells are exposed to inflammatory stimuli or low laminar shear stress (LSS), two factors commonly associated with atherosclerosis, B1R expression is induced. In vivo , B1R agonists stimulate inflammatory cell recruitment including neutrophils and macrophages. We now show in vitro that subjecting human aortic endothelial cells to low LSS enhances leukocyte adherence compared to physiological LSS. Moreover, this effect is enhanced in the presence of the cytokine interleukin‐1β, both conditions associated with increased endothelial B1R expression. Importantly treatment of endothelial cells with a B1R antagonist reduced cell adherence in cells exposed to low LSS but had no significant effect on the response under physiological LSS conditions. These results suggest that B1R may play an important role in inflammatory cell recruitment at sites of low LSS and targeting this protein might prove beneficial in the treatment of atherosclerosis. This work and KRM are funded by The British Heart Foundation