Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β: The role of prostanoids

Mei Chi Chang, Li Deh Lin, Jenny Zwei-Ching Chang, Chiung Fang Huang, Fu Hsiung Chuang, Jang Jaer Lee, Po Yuan Jeng, Tong Mei Wang, Jiiang Huei Jeng

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18 引文 斯高帕斯(Scopus)


Introduction: Vascular cell adhesion molecule (VCAM-1) plays a critical role in the inflammatory processes by stimulating the recruitment, extravasation, and migration of leukocytes. Its expression and regulation in the dental pulp is not well elucidated. Methods: Primary dental pulp cells were exposed to prostaglandin E 2 (PGE 2), prostaglandin F (PGF ), or interleukin 1β (IL-1β) with/without aspirin. VCAM-1 messenger RNA expression was analyzed by reverse transcriptase-polymerase chain reaction. Soluble VCAM-1 (sVCAM-1) in the culture medium was determined by enzyme-linked immunosorbent assay, and the number of viable cells was estimated by (3-[4,5-dimethylthiazol-2-yl]-2,5- diphenyltetrazolium bromide (MTT) assay. Results: IL-1β induced VCAM-1 gene expression of pulp cells. IL-1β also stimulated sVCAM-1 production. The IL-1β-induced sVCAM-1 production was not inhibited but rather enhanced by aspirin, a cyclooxygenase (COX) inhibitor. PGE 2 and PGF decreased the VCAM-1 expression and sVCAM-1 production of pulp cells. U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene), a mitogen-activated protein kinase kinase (MEK) inhibitor, attenuated IL-1β-induced sVCAM-1 production. However, no marked cytotoxicity was noted in these experimental conditions as analyzed by MTT assay. Conclusions: IL-1β may be involved in the pulpal inflammatory processes via stimulation of VCAM-1 expression and sVCAM-1 production. This event is not mediated by COX activation and prostanoid production but is associated with MEK signaling. PGE 2 and PGF may potentially regulate inflammatory processes by the inhibition of VCAM-1.

頁(從 - 到)774-779
期刊Journal of Endodontics
出版狀態已發佈 - 6月 2012

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