Effect of interleukin-1β on the ICAM-1 and MCP-1 expression of human dental pulp cells : Role of PI3K/Akt and MEK/ERK 1/2 Signaling and Cyclooxygenase
Date Issued
2014
Date
2014
Author(s)
Hung, Hsiu-Pin
Abstract
Aim: Interleukin-1β (IL-1β) is an important inflammatory mediator of the dental pulp. IL-1β may stimulate cyclooxygenase-2 (COX-2) and prostanoids production of pulp cells and affect the inflammatory and healing processes of dental pulp. However, the effects of IL-1β on Intercellular Adhesion Molecule-1 (ICAM-1) and Monocyte Chemotactic Factor-1 (MCP-1) of human dental pulp cells and its relation to PI3K/Akt and MEK/ERK 1/2 signaling and COX activation are still not clear.
Materials and Methods: Human dental pulp cells were treated with IL-1β with/without pretreatment and co-incubation by aspirin (a COX inhibitor) or LY294002 (a PI3K/Akt inhibitor) or U0126 ( a MEK/ERK 1/2 inhibitor) for different time periods. Viable cell number was evaluated by 3- (4,5-cimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The expression of ICAM-1 and MCP-1 mRNA was tested by reverse transcriptase – polymerase chain reaction (RT-PCR). ICAM-1 and MCP-1 protein expression was examined by western blotting. Phosphorylation of Akt and ERK 1/2 was measured by western blot.
Results: IL-1β showed little cytotoxicity to pulp cells. It stimulated ICAM-1 and MCP-1 mRNA and protein expression. Aspirin enhanced the IL-1β-induced ICAM-1 and MCP-1 mRNA expression and protein production. IL-1β rapidly activated Akt and ERK 1/2. Both LY294002 and U0126 attenuated the IL-1β-induced ICAM-1and MCP-1 mRNA expression.
Conclusions: These results reveal that IL-1β may involve in the pulpal inflammatory and healing processes by stimulation of ICAM-1and MCP-1 mRNA expression and protein production. These events are associated with differential activation of PI3K/Akt and MEK/ERK 1/2 signaling and COX. These results are useful for future treatment of pulpal inflammatory diseases.
Subjects
PI3K/Akt
MEK/ERK 1/2
環氧酶
牙髓細胞
發炎
介白素-1β
細胞間黏附分子-1
單核細胞趨化蛋白-1
SDGs
Type
thesis
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