Cytokine‐induced prostaglandin E₂ production and cyclooxygenase‐2 expression in dental pulp cells: downstream calcium signalling via activation of prostaglandin EP receptor

Abstract

Interleukin-1beta and TNF-alpha may stimulate PGE(2) production in dental pulp cells. Activation of prostaglandin EP receptors in dental pulp cells by PGE(2) may induce Ca(2+) signalling to regulate cellular biological activity during inflammation.

Effect of Tricalcium Aluminate on the Physicochemical Properties, Bioactivity, and Biocompatibility of Partially Stabilized Cements

“…A tissue explant technique was processed to cultivate dental pulp cells as described previously [22], [23]. Briefly, pulp tissues were minced into small pieces (approximately 1 mm 3 ) and then digested with 3 mg/mL collagenase type I (Sigma, St Louis, MO, USA) and 4 mg/mL dispase (Sigma, St Louis, MO, USA) for 1 h at 37°C.…”

Antiplatelet Effect of Catechol Is Related to Inhibition of Cyclooxygenase, Reactive Oxygen Species, ERK/p38 Signaling and Thromboxane A2 Production

“…Because we have found that IL-1β stimulates COX-2 expression and PGE 2 production by pulp cells [23], we further analyzed whether catechol may have anti-inflammatory effect and could inhibit IL-1β-induced PGE 2 production of pulp cells. Exposure to 50 and 100 µM catechol with/without IL-1β showed little effect on pulp cell morphology as compared with control pulp cells ( Figure 7A ), and minimal cytotoxicity with 50 and 100 µM catechol was observed ( Figure 7B ).…”

“…Vascular wall inflammation is related to platelet activation and constitutes a major pathogenic event in atherosclerosis [10]. Stimulation of COX-2 expression and PGE 2 production is crucial for tissue inflammation, pain response and cardiovascular disease [23], [47], [48]. Dental pulp is a specialized connective tissue popularly suffered from inflammatory and pain response, where IL-1β and PGE 2 are involved [22].…”

“…PGE 2 level of dental pulp and its induction by IL-1β is crucial to the pathogenesis of pulpitis and pulpal pain [22], [23]. To know the anti-inflammatory effect, we tested whether catechol may prevent IL-1β-induced COX-2 expression and PGE 2 production of pulp cells in this study.…”

Proinflammatory Cytokine Expression in Cyclooxygenase-2–deficient Primary Osteoblasts

“…Both IL-1␤ and TNF-␣ are known stimulators of PGE2 (22)(23)(24). Many of the proinflammatory effects of IL-1␤ and TNF-␣ such as IL-6 production are mediated by PGE2 (25).…”