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Author Spotlight: Enhancing Dental Pulp Research with Improved Mouse Models
Published on: October 27, 2023
Kallikrein Promotes Inflammation in Human Dental Pulp Cells Via Protease-Activated Receptor-1
Tomomi Hayama1, Naoto Kamio1, Tatsu Okabe1
1Department of Endodontics, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, 271-8587, Japan.
Abstract:
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 E2 . 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.
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