IL-1β-induced MCP-1 expression and secretion of human dental pulp cells is related to TAK1, MEK/ERK, and PI3K/Akt signaling pathways

Mei Chi Chang, Yi Ling Tsai, Hsiao Hua Chang, Sheng Yang Lee, Ming Shu Lee, Chun Wei Chang, Chiu Po Chan, Chien Yang Yeh, Ru Hsiu Cheng, Jiiang Huei Jeng

Research output: Contribution to journalArticle

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Abstract

Objective Interleukin-1β (IL-1β) is an inflammatory molecule of the dental pulp. IL-1β stimulates cyclooxygenase-2 (COX-2) and prostaglandins production of pulp cells and affects the pulpal inflammation and repair. However, the effects of IL-1β on Monocyte Chemotactic Factor-1 (MCP-1) of dental pulp cells and its relation to transforming growth factor β-activated kinase-1 (TAK1), PI3K/Akt, and MEK/ERK signaling and COX activation are not fully clear. Design Human dental pulp cells were exposed to IL-1β with/without pretreatment and co-incubation by aspirin (a COX inhibitor), 5z-7-oxozeaenol (a TAK1 inhibitor), LY294002 (a PI3K/Akt inhibitor) or U0126 (a MEK/ERK inhibitor). Viable cell number was evaluated by MTT assay. MCP-1 mRNA expression was tested by reverse transcriptase-polymerase chain reaction (RT-PCR). MCP-1 and COX-2 protein expression was studied by western blot. MCP-1 in the culture medium was measure by ELISA. Results IL-1β showed little cytotoxicity to pulp cells. It stimulated MCP-1 mRNA and protein expression and MCP-1 secretion. Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1β-induced MCP-1 expression. In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1β-induced MCP-1 secretion of pulp cells. Conclusion These results indicate that IL-1β may be involved in the pulpal inflammatory and healing processes by inducing MCP-1 expression and secretion. These events are related to differential activation of TAK1, PI3K/Akt and MEK/ERK 1/2 signaling and COX activation. These results are important for future pharmacologic intervention of pulpal inflammatory diseases.

Original languageEnglish
Pages (from-to)16-22
Number of pages7
JournalArchives of Oral Biology
Volume61
DOIs
Publication statusPublished - Jan 1 2016

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Dental Pulp
Mitogen-Activated Protein Kinase Kinases
Phosphatidylinositol 3-Kinases
Interleukin-1
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
Aspirin
Cyclooxygenase 2
Messenger RNA
Chemotactic Factors
Transforming Growth Factors
Reverse Transcriptase Polymerase Chain Reaction
Prostaglandins
Culture Media
Monocytes
Proteins
Phosphotransferases
Cell Count
Western Blotting
Enzyme-Linked Immunosorbent Assay
Inflammation

Keywords

  • Cyclooxygenase
  • Inflammation
  • Interleukin-1β
  • MCP-1
  • MEK/ERK
  • PI3K/Akt
  • Pulp
  • Signal transduction
  • TAK1

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Cell Biology
  • Dentistry(all)

Cite this

IL-1β-induced MCP-1 expression and secretion of human dental pulp cells is related to TAK1, MEK/ERK, and PI3K/Akt signaling pathways. / Chang, Mei Chi; Tsai, Yi Ling; Chang, Hsiao Hua; Lee, Sheng Yang; Lee, Ming Shu; Chang, Chun Wei; Chan, Chiu Po; Yeh, Chien Yang; Cheng, Ru Hsiu; Jeng, Jiiang Huei.

In: Archives of Oral Biology, Vol. 61, 01.01.2016, p. 16-22.

Research output: Contribution to journalArticle

Chang, Mei Chi ; Tsai, Yi Ling ; Chang, Hsiao Hua ; Lee, Sheng Yang ; Lee, Ming Shu ; Chang, Chun Wei ; Chan, Chiu Po ; Yeh, Chien Yang ; Cheng, Ru Hsiu ; Jeng, Jiiang Huei. / IL-1β-induced MCP-1 expression and secretion of human dental pulp cells is related to TAK1, MEK/ERK, and PI3K/Akt signaling pathways. In: Archives of Oral Biology. 2016 ; Vol. 61. pp. 16-22.
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abstract = "Objective Interleukin-1β (IL-1β) is an inflammatory molecule of the dental pulp. IL-1β stimulates cyclooxygenase-2 (COX-2) and prostaglandins production of pulp cells and affects the pulpal inflammation and repair. However, the effects of IL-1β on Monocyte Chemotactic Factor-1 (MCP-1) of dental pulp cells and its relation to transforming growth factor β-activated kinase-1 (TAK1), PI3K/Akt, and MEK/ERK signaling and COX activation are not fully clear. Design Human dental pulp cells were exposed to IL-1β with/without pretreatment and co-incubation by aspirin (a COX inhibitor), 5z-7-oxozeaenol (a TAK1 inhibitor), LY294002 (a PI3K/Akt inhibitor) or U0126 (a MEK/ERK inhibitor). Viable cell number was evaluated by MTT assay. MCP-1 mRNA expression was tested by reverse transcriptase-polymerase chain reaction (RT-PCR). MCP-1 and COX-2 protein expression was studied by western blot. MCP-1 in the culture medium was measure by ELISA. Results IL-1β showed little cytotoxicity to pulp cells. It stimulated MCP-1 mRNA and protein expression and MCP-1 secretion. Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1β-induced MCP-1 expression. In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1β-induced MCP-1 secretion of pulp cells. Conclusion These results indicate that IL-1β may be involved in the pulpal inflammatory and healing processes by inducing MCP-1 expression and secretion. These events are related to differential activation of TAK1, PI3K/Akt and MEK/ERK 1/2 signaling and COX activation. These results are important for future pharmacologic intervention of pulpal inflammatory diseases.",
keywords = "Cyclooxygenase, Inflammation, Interleukin-1β, MCP-1, MEK/ERK, PI3K/Akt, Pulp, Signal transduction, TAK1",
author = "Chang, {Mei Chi} and Tsai, {Yi Ling} and Chang, {Hsiao Hua} and Lee, {Sheng Yang} and Lee, {Ming Shu} and Chang, {Chun Wei} and Chan, {Chiu Po} and Yeh, {Chien Yang} and Cheng, {Ru Hsiu} and Jeng, {Jiiang Huei}",
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T1 - IL-1β-induced MCP-1 expression and secretion of human dental pulp cells is related to TAK1, MEK/ERK, and PI3K/Akt signaling pathways

AU - Chang, Mei Chi

AU - Tsai, Yi Ling

AU - Chang, Hsiao Hua

AU - Lee, Sheng Yang

AU - Lee, Ming Shu

AU - Chang, Chun Wei

AU - Chan, Chiu Po

AU - Yeh, Chien Yang

AU - Cheng, Ru Hsiu

AU - Jeng, Jiiang Huei

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Objective Interleukin-1β (IL-1β) is an inflammatory molecule of the dental pulp. IL-1β stimulates cyclooxygenase-2 (COX-2) and prostaglandins production of pulp cells and affects the pulpal inflammation and repair. However, the effects of IL-1β on Monocyte Chemotactic Factor-1 (MCP-1) of dental pulp cells and its relation to transforming growth factor β-activated kinase-1 (TAK1), PI3K/Akt, and MEK/ERK signaling and COX activation are not fully clear. Design Human dental pulp cells were exposed to IL-1β with/without pretreatment and co-incubation by aspirin (a COX inhibitor), 5z-7-oxozeaenol (a TAK1 inhibitor), LY294002 (a PI3K/Akt inhibitor) or U0126 (a MEK/ERK inhibitor). Viable cell number was evaluated by MTT assay. MCP-1 mRNA expression was tested by reverse transcriptase-polymerase chain reaction (RT-PCR). MCP-1 and COX-2 protein expression was studied by western blot. MCP-1 in the culture medium was measure by ELISA. Results IL-1β showed little cytotoxicity to pulp cells. It stimulated MCP-1 mRNA and protein expression and MCP-1 secretion. Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1β-induced MCP-1 expression. In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1β-induced MCP-1 secretion of pulp cells. Conclusion These results indicate that IL-1β may be involved in the pulpal inflammatory and healing processes by inducing MCP-1 expression and secretion. These events are related to differential activation of TAK1, PI3K/Akt and MEK/ERK 1/2 signaling and COX activation. These results are important for future pharmacologic intervention of pulpal inflammatory diseases.

AB - Objective Interleukin-1β (IL-1β) is an inflammatory molecule of the dental pulp. IL-1β stimulates cyclooxygenase-2 (COX-2) and prostaglandins production of pulp cells and affects the pulpal inflammation and repair. However, the effects of IL-1β on Monocyte Chemotactic Factor-1 (MCP-1) of dental pulp cells and its relation to transforming growth factor β-activated kinase-1 (TAK1), PI3K/Akt, and MEK/ERK signaling and COX activation are not fully clear. Design Human dental pulp cells were exposed to IL-1β with/without pretreatment and co-incubation by aspirin (a COX inhibitor), 5z-7-oxozeaenol (a TAK1 inhibitor), LY294002 (a PI3K/Akt inhibitor) or U0126 (a MEK/ERK inhibitor). Viable cell number was evaluated by MTT assay. MCP-1 mRNA expression was tested by reverse transcriptase-polymerase chain reaction (RT-PCR). MCP-1 and COX-2 protein expression was studied by western blot. MCP-1 in the culture medium was measure by ELISA. Results IL-1β showed little cytotoxicity to pulp cells. It stimulated MCP-1 mRNA and protein expression and MCP-1 secretion. Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1β-induced MCP-1 expression. In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1β-induced MCP-1 secretion of pulp cells. Conclusion These results indicate that IL-1β may be involved in the pulpal inflammatory and healing processes by inducing MCP-1 expression and secretion. These events are related to differential activation of TAK1, PI3K/Akt and MEK/ERK 1/2 signaling and COX activation. These results are important for future pharmacologic intervention of pulpal inflammatory diseases.

KW - Cyclooxygenase

KW - Inflammation

KW - Interleukin-1β

KW - MCP-1

KW - MEK/ERK

KW - PI3K/Akt

KW - Pulp

KW - Signal transduction

KW - TAK1

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