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Kallikrein Promotes Inflammation in Human Dental Pulp Cells Via Protease‐Activated Receptor‐1
Author(s) -
Hayama Tomomi,
Kamio Naoto,
Okabe Tatsu,
Muromachi Koichiro,
Matsushima Kiyoshi
Publication year - 2016
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.25437
Subject(s) - kallikrein , protease activated receptor 2 , protease activated receptor , receptor , chemistry , plasmin , bradykinin , inflammation , microbiology and biotechnology , thrombin , serine protease , high molecular weight kininogen , protease , biochemistry , kininogen , biology , enzyme , immunology , enzyme linked receptor , platelet
Plasma kallikrein (KLKB1), a serine protease, cleaves high‐molecular weight kininogen to produce bradykinin, a potent vasodilator and pro‐inflammatory peptide. In addition, KLKB1 activates plasminogen and other leukocyte and blood coagulation factors and processes pro‐enkephalin, prorenin, and C3. KLKB1 has also been shown to cleave protease‐activated receptors in vascular smooth muscle cells to regulate the expression of epidermal growth factor receptor. In this study, we investigated KLKB1‐dependent inflammation and activation of protease‐activated receptor‐1 in human dental pulp cells. These cells responded to KLKB1 stimulation by increasing intracellular Ca 2+ , upregulating cyclooxygenase‐2, and secreting prostaglandin E 2 . Remarkably, SCH79797, an antagonist of protease‐activated receptor‐1, blocked these effects. Thus, these data indicate that KLKB1 induces inflammatory reactions in human dental tissues via protease‐activated receptor 1. J. Cell. Biochem. 117: 1522–1528, 2016. © 2015 Wiley Periodicals, Inc.