Involvement of PKC, p38 MAPK and AP-2 in IL-1β-induced expression of cyclooxygenase-2 in human pulmonary epithelial cells

Ping Chen, Ying Cai, Zhi Gang Yang, Rui Zhou, Guang Shen Zhang, Frederick Domann, Xiang Fang

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Objective: The aim of this study was to identify the signal molecules involved in IL-1β-induced expression of cyclooxygenase (COX)-2 in human pulmonary epithelial (A549) cells. Methods: A549 cells were stimulated with IL-1β in the presence or absence of H-7 (a protein kinase C inhibitor), SB203580 (a p38 mitogen-activated protein kinase inhibitor) and PD098059 (a mitogen-activated and extracellular regulated kinase kinase (MEK1) inhibitor). The A549 cells were also transfected with adenovirus vector encoding activator protein (AP)-2α, or a plasmid containing a dominant-negative gene (AP-2Δ), in the presence or absence of IL-1β. Results: IL-1β induced expression of the COX-2 mRNA and protein in A549 cells in a time- and dose-dependent manner. SB203580 and H-7, but not PD098059, inhibited IL-1β-induced expression of COX-2 protein. Overexpression of AP-2α increased expression of the COX-2 protein, whereas AP-2Δ decreased IL-1β-induced COX-2 expression. Conclusion: Protein kinase C, p38 mitogen-activated protein kinase and transcriptional factor AP-2α may play important roles in regulating IL-1β-induced COX-2 expression in human pulmonary epithelial cells.

Original languageEnglish (US)
Pages (from-to)18-23
Number of pages6
JournalRespirology
Volume11
Issue number1
DOIs
StatePublished - Jan 2006
Externally publishedYes

Fingerprint

p38 Mitogen-Activated Protein Kinases
Cyclooxygenase 2
Interleukin-1
Epithelial Cells
Lung
Proteins
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Protein Kinase Inhibitors
Protein Kinase C
Phosphotransferases
Dominant Genes
Protein C Inhibitor
Mitogens
Adenoviridae
Plasmids
Messenger RNA
A549 Cells

Keywords

  • Activator protein-2
  • Cyclooxygenase-2
  • Mitogen-activated and extracellular regulated kinase kinase 1
  • Mitogen-activated protein kinase
  • Protein kinase C

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Involvement of PKC, p38 MAPK and AP-2 in IL-1β-induced expression of cyclooxygenase-2 in human pulmonary epithelial cells. / Chen, Ping; Cai, Ying; Yang, Zhi Gang; Zhou, Rui; Zhang, Guang Shen; Domann, Frederick; Fang, Xiang.

In: Respirology, Vol. 11, No. 1, 01.2006, p. 18-23.

Research output: Contribution to journalArticle

Chen, Ping ; Cai, Ying ; Yang, Zhi Gang ; Zhou, Rui ; Zhang, Guang Shen ; Domann, Frederick ; Fang, Xiang. / Involvement of PKC, p38 MAPK and AP-2 in IL-1β-induced expression of cyclooxygenase-2 in human pulmonary epithelial cells. In: Respirology. 2006 ; Vol. 11, No. 1. pp. 18-23.
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abstract = "Objective: The aim of this study was to identify the signal molecules involved in IL-1β-induced expression of cyclooxygenase (COX)-2 in human pulmonary epithelial (A549) cells. Methods: A549 cells were stimulated with IL-1β in the presence or absence of H-7 (a protein kinase C inhibitor), SB203580 (a p38 mitogen-activated protein kinase inhibitor) and PD098059 (a mitogen-activated and extracellular regulated kinase kinase (MEK1) inhibitor). The A549 cells were also transfected with adenovirus vector encoding activator protein (AP)-2α, or a plasmid containing a dominant-negative gene (AP-2Δ), in the presence or absence of IL-1β. Results: IL-1β induced expression of the COX-2 mRNA and protein in A549 cells in a time- and dose-dependent manner. SB203580 and H-7, but not PD098059, inhibited IL-1β-induced expression of COX-2 protein. Overexpression of AP-2α increased expression of the COX-2 protein, whereas AP-2Δ decreased IL-1β-induced COX-2 expression. Conclusion: Protein kinase C, p38 mitogen-activated protein kinase and transcriptional factor AP-2α may play important roles in regulating IL-1β-induced COX-2 expression in human pulmonary epithelial cells.",
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AU - Zhang, Guang Shen

AU - Domann, Frederick

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N2 - Objective: The aim of this study was to identify the signal molecules involved in IL-1β-induced expression of cyclooxygenase (COX)-2 in human pulmonary epithelial (A549) cells. Methods: A549 cells were stimulated with IL-1β in the presence or absence of H-7 (a protein kinase C inhibitor), SB203580 (a p38 mitogen-activated protein kinase inhibitor) and PD098059 (a mitogen-activated and extracellular regulated kinase kinase (MEK1) inhibitor). The A549 cells were also transfected with adenovirus vector encoding activator protein (AP)-2α, or a plasmid containing a dominant-negative gene (AP-2Δ), in the presence or absence of IL-1β. Results: IL-1β induced expression of the COX-2 mRNA and protein in A549 cells in a time- and dose-dependent manner. SB203580 and H-7, but not PD098059, inhibited IL-1β-induced expression of COX-2 protein. Overexpression of AP-2α increased expression of the COX-2 protein, whereas AP-2Δ decreased IL-1β-induced COX-2 expression. Conclusion: Protein kinase C, p38 mitogen-activated protein kinase and transcriptional factor AP-2α may play important roles in regulating IL-1β-induced COX-2 expression in human pulmonary epithelial cells.

AB - Objective: The aim of this study was to identify the signal molecules involved in IL-1β-induced expression of cyclooxygenase (COX)-2 in human pulmonary epithelial (A549) cells. Methods: A549 cells were stimulated with IL-1β in the presence or absence of H-7 (a protein kinase C inhibitor), SB203580 (a p38 mitogen-activated protein kinase inhibitor) and PD098059 (a mitogen-activated and extracellular regulated kinase kinase (MEK1) inhibitor). The A549 cells were also transfected with adenovirus vector encoding activator protein (AP)-2α, or a plasmid containing a dominant-negative gene (AP-2Δ), in the presence or absence of IL-1β. Results: IL-1β induced expression of the COX-2 mRNA and protein in A549 cells in a time- and dose-dependent manner. SB203580 and H-7, but not PD098059, inhibited IL-1β-induced expression of COX-2 protein. Overexpression of AP-2α increased expression of the COX-2 protein, whereas AP-2Δ decreased IL-1β-induced COX-2 expression. Conclusion: Protein kinase C, p38 mitogen-activated protein kinase and transcriptional factor AP-2α may play important roles in regulating IL-1β-induced COX-2 expression in human pulmonary epithelial cells.

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