Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-α- and dexamethasone-stimulated human periodontal ligament cells
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- 作者：Hwa-Jeong Lee ; Jin-Woo Cho ; Sang-Cheol Kim ; Kyung-Hwa Kang ; Sun-Kyung Lee ; Sung-Hee Pi ; Suk-Keun Lee and Eun-Cheol Kim
- 关键词：IL-8 ; ICAM-1 ; TNF-α ; Dexamethasone ; Human periodontal ligament cells ; MAP kinase ; NF-κ ; B
- 刊名：Cytokine
- 出版年：2006
- 出版时间：July 2006
- 年：2006
- 卷：35
- 期：1-2
- 页码：67-76
- 全文大小：768 K
文摘
Orthodontic tooth movement is recognized as a pro-inflammatory stressor of human periodontal ligament (hPDL) cells. However, the cell-signaling pathways linking interleukin-8 (IL-8), intercellular adhesion molecule-1 (ICAM-1), pro-inflammatory cytokines, and dexamethasone in hPDL cells have not been well elucidated. In this study, we investigated the role of mitogen-activated protein (MAP) kinases in dexamethasone- and TNF-α-induced IL-8 and ICAM-1 expression in hPDL cells. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. MAP kinase activation and IκB degradation were determined by Western blot analysis, and ICAM-1 expression was determined by RT-PCR and FACS analysis. TNF-α increased IL-8 mRNA expression and protein secretion in a dose- and time-dependent manner. Dexamethasone suppressed TNF-α-induced IL-8 production in a dose-dependent manner. In addition, dexamethasone inhibited TNF-α-induced phosphorylation of p38 MAP kinase and extracellular-regulated kinases (ERKs), IκB degradation, and NF-κB activation. Selective inhibitors for ERKs and p38 attenuated TNF-α-induced IL-8 and ICAM-1 expression in the presence and absence of dexamethasone, indicating that MAP kinases play a role in the response of hDPL cells to TNF-α. Furthermore, these results suggest that inflammatory cytokine- and dexamethasone-induced IL-8 and ICAM-1, produced via a MAP kinase pathway, may serve as an important mediator of PDL immunoregulation involved in bone remodeling during orthodontic tooth movement.