15-deoxy-Δ12,14-prostaglandin J2 inhibits the IL-1β-induced expression of granulocyte-macrophage colony-stimulating factor in BEAS-2B bronchial epithelial cells

Mika Kumagai, Tadaatsu Imaizumi, Katsuhiko Suzuki, Hidemi Yoshida, Shingo Takanashi, Ken Okumura, Kazuo Sugawara, Kei Satoh

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is an agonist for peroxisome proliferator-activated receptor-γ (PPAR-γ), which plays an important role in various biological processes including inflammatory responses. We have addressed the effect of 15d-PGJ2 on the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in a cell line derived from human bronchial epithelial cells (BEAS-2B). Besides being a hematopoietic growth factor, GM-CSF activates mature leukocytes and is involved in regulation of inflammatory responses. Cultures of BEAS-2B were stimulated with interleukin-1β (IL-1β), and the expressions of GM-CSF mRNA and protein were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. IL-1β stimulated the expression of GM-CSF in BEAS-2B cells in concentration- and time-dependent manners. When the cells were pretreated with 15d-PGJ2 for 1 hour, the IL-1β-induced GM-CSF expression was inhibited in a concentration-dependent manner (2-50 μM). Ciglitazone, another agonist of PPAR-γ, did not affect the IL-1β-induced GM-CSF expression in BEAS-2B cells. A PPAR-γ antagonist, bisphenol A diglycide ether (BADGE), did not reverse the inhibitory effects of 15d-PGJ2 on GM-CSF expression. 15d-PGJ2 regulates GM-CSF expression in the bronchial epithelium, which may be mediated through a mechanism unrelated to PPAR-γ.

Original languageEnglish
Pages (from-to)69-76
Number of pages8
JournalTohoku Journal of Experimental Medicine
Volume202
Issue number2
DOIs
Publication statusPublished - 2004 Feb
Externally publishedYes

Fingerprint

Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-1
Epithelial Cells
Peroxisome Proliferator-Activated Receptors
Biological Phenomena
Immunosorbents
15-deoxy-delta(12,14)-prostaglandin J2
Polymerase chain reaction
Transcription
Ether
Reverse Transcription
Assays
Intercellular Signaling Peptides and Proteins
Leukocytes
Epithelium
Enzyme-Linked Immunosorbent Assay
Cells
Cell Line
Polymerase Chain Reaction
Messenger RNA

Keywords

  • 15d-PGJ
  • BADGE
  • BEAS-2B
  • GM-CSF
  • IL-1β

ASJC Scopus subject areas

  • Medicine(all)

Cite this

15-deoxy-Δ12,14-prostaglandin J2 inhibits the IL-1β-induced expression of granulocyte-macrophage colony-stimulating factor in BEAS-2B bronchial epithelial cells. / Kumagai, Mika; Imaizumi, Tadaatsu; Suzuki, Katsuhiko; Yoshida, Hidemi; Takanashi, Shingo; Okumura, Ken; Sugawara, Kazuo; Satoh, Kei.

In: Tohoku Journal of Experimental Medicine, Vol. 202, No. 2, 02.2004, p. 69-76.

Research output: Contribution to journalArticle

Kumagai, Mika ; Imaizumi, Tadaatsu ; Suzuki, Katsuhiko ; Yoshida, Hidemi ; Takanashi, Shingo ; Okumura, Ken ; Sugawara, Kazuo ; Satoh, Kei. / 15-deoxy-Δ12,14-prostaglandin J2 inhibits the IL-1β-induced expression of granulocyte-macrophage colony-stimulating factor in BEAS-2B bronchial epithelial cells. In: Tohoku Journal of Experimental Medicine. 2004 ; Vol. 202, No. 2. pp. 69-76.
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abstract = "15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is an agonist for peroxisome proliferator-activated receptor-γ (PPAR-γ), which plays an important role in various biological processes including inflammatory responses. We have addressed the effect of 15d-PGJ2 on the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in a cell line derived from human bronchial epithelial cells (BEAS-2B). Besides being a hematopoietic growth factor, GM-CSF activates mature leukocytes and is involved in regulation of inflammatory responses. Cultures of BEAS-2B were stimulated with interleukin-1β (IL-1β), and the expressions of GM-CSF mRNA and protein were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. IL-1β stimulated the expression of GM-CSF in BEAS-2B cells in concentration- and time-dependent manners. When the cells were pretreated with 15d-PGJ2 for 1 hour, the IL-1β-induced GM-CSF expression was inhibited in a concentration-dependent manner (2-50 μM). Ciglitazone, another agonist of PPAR-γ, did not affect the IL-1β-induced GM-CSF expression in BEAS-2B cells. A PPAR-γ antagonist, bisphenol A diglycide ether (BADGE), did not reverse the inhibitory effects of 15d-PGJ2 on GM-CSF expression. 15d-PGJ2 regulates GM-CSF expression in the bronchial epithelium, which may be mediated through a mechanism unrelated to PPAR-γ.",
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T1 - 15-deoxy-Δ12,14-prostaglandin J2 inhibits the IL-1β-induced expression of granulocyte-macrophage colony-stimulating factor in BEAS-2B bronchial epithelial cells

AU - Kumagai, Mika

AU - Imaizumi, Tadaatsu

AU - Suzuki, Katsuhiko

AU - Yoshida, Hidemi

AU - Takanashi, Shingo

AU - Okumura, Ken

AU - Sugawara, Kazuo

AU - Satoh, Kei

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