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Effects of TNF-α on the expression of monocyte chemoattractant protein-1 and the corresponding signal transduction pathway in dental follicle cells

By Ying-chun BI, Ming JIANG, Peng LIU and Zuo-lin JIN

Abstract

Objective To study the effect of different concentration of tumor necrosis factor-α(TNF-α) on the expression of monocyte chemoattractant protein-1(MCP-1) and the corresponding signal transduction pathway in human dental follicle cells.Methods The 5th passage of human dental follicle cells were co-incubated with 0(control group),5,10,25,50 and 100 ng/ml TNF-α,respectively,for 6 hours.The contents of MCP-1 in the supernatant were measured by using sandwich ELISA,and the expression of MCP-1 mRNA was determined by reverses transcription polymerase chain reaction(RT-PCR).Furthermore,to determine the corresponding signal transduction pathway,the 5th passage of human dental follicle cells were incubated with 25 μmol/L SB203580 to inhibit p38 mitogen-activated protein kinase(p38MARK),with 50 μmol/L PD98059 to inhibit extracellular signal-regulated kinases(ERK),and with 15 μmol/L SP600125 to inhibit c-Jun N-terminal kinases(JNK) for 30min,then incubated with TNF-α(10ng/ml) for 6h.MCP-1 mRNA was detected by RT-PCR.Results The results of ELISA revealed that 10-100 ng/ml of TNF-α enhanced MCP-1 secretion(P < 0.05) compared to that in human dental follicle cells without TNF-α treatment.Cells treated with 10-50 ng/ml of TNF-α showed a significant increase of MCP-1 mRNA expression(P < 0.05),and the action was inhibited by SP600125,which was the special inhibitor of c-Jun N-terminal kinase(JNK).Conclusion TNF-α may enhance MCP-1 gene expression and secretion in human dental follicle cells,and the activation of JNK signal transduction pathway is required in this process

Topics: dental sca; tumor necrosis factor-alpha; monocyte chemokine CCL2, Medicine (General), R5-920, Medicine, R, DOAJ:Medicine (General), DOAJ:Health Sciences
Publisher: Editorial Board of Medical Journal of Chinese People's Liberation Army
Year: 2011
OAI identifier: oai:doaj.org/article:1d4dc8bd51664ac7afba908318925089
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