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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.

Macrophage migration inhibitory factor (MIF) has emerged as an essential proinflammatory cytokine in inflammatory and immune responses. We investigated the expression of MIF in human dental pulp tissue and the function of MIF in human dental pulp fibroblast-like cells. MIF was expressed in areas of dental pulp characterized by a robust inflammatory response, for instance, in human dental pulp tissues that exhibited pathological signs of purulent inflammation. MIF stimulated the expression of prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA and prostaglandin E 2 production in human dental pulp fibroblast-like cells. These effects of MIF on the expression of PTGS2 mRNA and prostaglandin E 2 production were attenuated in the presence of the CXCR2 and CXCR4 antagonists SCH527123 and WZ811. These results suggest that MIF is involved in inflammation by activating CXCR2 and CXCR4 in human dental pulp.

Purpose: In this study, to elucidate the ability of Ga-Al-As laser treatment to induce hard tissue formation, human dental pulp cells (hDPCs) stimulated with high concentration prostaglandin E 2 (PGE 2), which inhibits hard tissue formation, were irradiated with lasers at 660 or 810 nm. Differences in the molecular mechanisms underlying hard tissue formation using Ga-Al-As lasers at these wavelengths, including signaling via the bone morphogenetic protein(BMP)/SMAD pathway, were examined and compared. Methods: hDPCs were harvested from third molars extracted under aseptic conditions from 20-year-old patients undergoing orthodontic treatment. hDPCs were cultured for up to 30 days. After adding PGE 2 , hDPCs were irradiated with a Ga-Al-As laser at an output of 300 mW and wavelengths of 660 or 810 nm, approximately 10 cm above the culture supernatant. The laser irradiation time period was set to 600 seconds. BMP2, phosphorylated-(p-) SMAD1/5/8 and SMAD6 production were evaluated and calcified nodules stained. Results: Ga-Al-As laser treatment resulted in decreased SMAD6 mRNA and increased protein expression of p-SMAD1/5/8 in groups irradiated at both wavelengths, compared with hDPCs stimulated with PGE 2. Moreover, those irradiated at 810 nm exhibited lower BMP2 mRNA expression, but no definite difference in SMAD6 protein expression, compared with cells stimulated with PGE 2. Conclusion: Using Ga-Al-As lasers at the same output power, our results suggest that irradiation at 660 nm enhanced the ability of hDPCs to form hard tissue by suppressing SMAD6 expression; however, irradiation at 810 nm enhanced hard tissue generation via a different route that did not involve BMP2 and SMAD6.