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Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells.
Cytokine. 2006 Jul; 35(1-2):67-76.C

Abstract

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-alpha-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 IkappaB degradation were determined by Western blot analysis, and ICAM-1 expression was determined by RT-PCR and FACS analysis. TNF-alpha increased IL-8 mRNA expression and protein secretion in a dose- and time-dependent manner. Dexamethasone suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. In addition, dexamethasone inhibited TNF-alpha-induced phosphorylation of p38 MAP kinase and extracellular-regulated kinases (ERKs), IkappaB degradation, and NF-kappaB activation. Selective inhibitors for ERKs and p38 attenuated TNF-alpha-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-alpha. 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.

Authors+Show Affiliations

Department of Oral and Maxillofacial Pathology, College of Dentistry, Wonkwang University, Iksan, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16949835

Citation

Lee, Hwa-Jeong, et al. "Roles of P38 and ERK MAP Kinases in IL-8 Expression in TNF-alpha- and Dexamethasone-stimulated Human Periodontal Ligament Cells." Cytokine, vol. 35, no. 1-2, 2006, pp. 67-76.
Lee HJ, Cho JW, Kim SC, et al. Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells. Cytokine. 2006;35(1-2):67-76.
Lee, H. J., Cho, J. W., Kim, S. C., Kang, K. H., Lee, S. K., Pi, S. H., Lee, S. K., & Kim, E. C. (2006). Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells. Cytokine, 35(1-2), 67-76.
Lee HJ, et al. Roles of P38 and ERK MAP Kinases in IL-8 Expression in TNF-alpha- and Dexamethasone-stimulated Human Periodontal Ligament Cells. Cytokine. 2006;35(1-2):67-76. PubMed PMID: 16949835.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells. AU - Lee,Hwa-Jeong, AU - Cho,Jin-Woo, AU - Kim,Sang-Cheol, AU - Kang,Kyung-Hwa, AU - Lee,Sun-Kyung, AU - Pi,Sung-Hee, AU - Lee,Suk-Keun, AU - Kim,Eun-Cheol, Y1 - 2006/09/01/ PY - 2006/02/01/received PY - 2006/07/03/revised PY - 2006/07/26/accepted PY - 2006/9/5/pubmed PY - 2006/12/15/medline PY - 2006/9/5/entrez SP - 67 EP - 76 JF - Cytokine JO - Cytokine VL - 35 IS - 1-2 N2 - 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-alpha-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 IkappaB degradation were determined by Western blot analysis, and ICAM-1 expression was determined by RT-PCR and FACS analysis. TNF-alpha increased IL-8 mRNA expression and protein secretion in a dose- and time-dependent manner. Dexamethasone suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. In addition, dexamethasone inhibited TNF-alpha-induced phosphorylation of p38 MAP kinase and extracellular-regulated kinases (ERKs), IkappaB degradation, and NF-kappaB activation. Selective inhibitors for ERKs and p38 attenuated TNF-alpha-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-alpha. 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. SN - 1043-4666 UR - https://www.unboundmedicine.com/medline/citation/16949835/Roles_of_p38_and_ERK_MAP_kinases_in_IL_8_expression_in_TNF_alpha__and_dexamethasone_stimulated_human_periodontal_ligament_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-4666(06)00216-X DB - PRIME DP - Unbound Medicine ER -