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Influence of Kinin Peptides on Monocyte–Endothelial Cell Adhesion
Author(s) -
GuevaraLora Ibeth,
Stalinska Krystyna,
Augustynek Bartlomiej,
LabedzMaslowska Anna
Publication year - 2014
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24870
Subject(s) - kinin , proinflammatory cytokine , bradykinin , microbiology and biotechnology , cell adhesion , monocyte , endothelial stem cell , cell adhesion molecule , chemistry , biology , receptor , inflammation , immunology , cell , biochemistry , in vitro
Adhesion of leukocytes to vascular endothelium in response to proinflammatory mediators is an important component of the overall inflammatory reaction. In the current work, we used a retinoic acid‐differentiated human promonocytic cell line, U937 and a human microvascular endothelial cell line, HMEC‐1 to analyze the effect of the potent pro‐inflammatory bradykinin‐related peptides (kinins) on cell adhesion. Bradykinin (BK) and kinin metabolites without the C‐terminal arginine residue enhanced adhesion of the monocyte‐like cells to fibronectin and to the HMEC‐1 cells. Expression of adhesion proteins on the surface of both cell types was altered by the kinin peptides. In the monocyte‐like cells, expression of CD11b, a subunit of Mac‐1 integrin, was significantly increased whilst in the endothelial cells, a strong increase in the production of intercellular adhesion molecule 1 (ICAM‐1) was observed. The positive bradykinin‐induced effect on the cell–cell interaction was reversed by a carboxypeptidase inhibitor (MGTA), hence we suspected a significant role of the des‐Arg kinin metabolites, which acted through the kinin receptor type 1. Indeed, the expression of this receptor was up‐regulated not only by agonists but also by interferon‐γ and bradykinin. Kinin peptides also regulated signal transducer and activator of transcription proteins (STATs) activated by cytokines. Taken together, the above observations support our hypothesis that kinins stimulate monocyte adhesion to the vessel wall, especially during pathological states of the circulatory system accompanied by proinflammatory cytokine release. J. Cell. Biochem. 115: 1985–1995, 2014. © 2014 Wiley Periodicals, Inc.