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Basic Research| Volume 35, ISSUE 4, P508-512, April 2009

Prostaglandin F-Induced Interleukin-8 Production in Human Dental Pulp Cells Is Associated With MEK/ERK Signaling

  • Mei-Chi Chang
    Affiliations
    Biomedical Science Team, Chang Gung Institute of Technology, Taoyuan, Taiwan
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  • Hsiao-Hua Chang
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Mon-Ying Lee
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Chiu-Chun Lin
    Affiliations
    Department of Dentistry, Chang Gung Memorial Hospital, Kaohsiung, Taiwan
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  • Hung-Wei Yeh
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Ting-Ting Yang
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Po-Shuen Lin
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Wan-Yu Tseng
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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  • Jiiang-Huei Jeng
    Correspondence
    Address requests for reprints to Professor Jiiang-Huei Jeng, Department of Dentistry and School of Dentistry, National Taiwan University Hospital and National Taiwan University, Medical College, No 1, Chang-Te Street, Taipei, Taiwan.
    Affiliations
    Laboratory of Pharmacology, Toxicology & Pulp Biology, Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan
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Published:February 24, 2009DOI:https://doi.org/10.1016/j.joen.2008.12.023

      Abstract

      Prostaglandin F2alpha (PGF) and interleukin-1beta (IL-1β) levels are elevated in inflamed dental pulp. The roles of IL-1β and PGF in the pathogenesis of pulpal inflammation await investigation. We found that IL-1β stimulated PGF production of human dental pulp cells. IL-1β and PGF (0.5–10 μmol/L) also induced IL-8 production and mRNA expression in pulp cells. Aspirin inhibited IL-1β–induced PGF, but not IL-8 production. PGF-induced IL-8 production and mRNA expression were inhibited by U0126 (an inhibitor of mitogen-activated protein kinase kinase [MEK1/2]) inhibitor), whereas SQ22536 (an adenylate cyclase inhibitor) enhanced this event. These results indicate that IL-1β–induced IL-8 production in pulp cells is not mainly via direct activation of cyclooxygenase and PGF generation. PGF-induced IL-8 production is possibly via activation of MEK/extracellular signal-regulated kinase signaling, but not by activation of adenylate cyclase. IL-1β and PGF might involve the pathogenesis of pulpal inflammation via induction of IL-8 production.

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