The 15-deoxy-δ12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via enhancement of the platelet‑activating factor acetylhydrolase activity in human retinal pigment epithelial cells

  • Authors:
    • Won-Kyo Jung
    • Chang-Min Lee
    • Dae-Sung Lee
    • Giyoun Na
    • Da-Young Lee
    • Inhak Choi
    • Sae-Gwang Park
    • Su-Kil Seo
    • Jae-Wook Yang
    • Jung Sik Choi
    • Young-Min Lee
    • Won Sun Park
    • Il-Whan Choi
  • View Affiliations

  • Published online on: December 13, 2013     https://doi.org/10.3892/ijmm.2013.1588
  • Pages: 449-456
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Abstract

A well-recognized natural ligand of PPARγ, 15-deoxy-δ12,14-prostaglandin J2 (15d-PGJ2) possesses immunomodulatory properties. The aim of this study was to elucidate whether 15d-PGJ2 was able to attenuate lipopolysaccharide (LPS)-induced inflammatory responses in human retinal pigment epithelial (RPE) cells, which are involved in ocular immune responses. In addition, we examined whether the platelet activating factor (PAF) is associated with the anti-inflammatory activity of 15d-PGJ2. ARPE19 cells treated with varying concentrations of 15d-PGJ2 and a PAF antagonist (CV3988) were used in this study. The activity of PAF-acetylhydrolase (PAF-AH) was assayed by treatment with 15d-PGJ2 and CV3988 in the presence of LPS. 15d-PGJ2 and CV3988 inhibited the LPS-induced mRNA expression and protein production of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) in ARPE19 cells. These effects resulting from 15d-PGJ2 were not abrogated by the PPARγ antagonist, indicating that the actions were PPARγ-independent. Furthermore, 15d-PGJ2 and CV3988 enhanced the PAF-AH activity. Additionally, 15d-PGJ2 inhibited the phosphorylation of the extracellular signal-regulated kinase (ERK) and the activation of nuclear transcription factor-κB (NF-κB). These results demonstrated that 15d-PGJ2 reduced LPS-stimulated inflammatory responses in ARPE19 cells by enhancing the PAH-AH activity. These results suggest that 15d-PGJ2 may have potent anti-inflammatory activity against ocular inflammation.
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2014-February
Volume 33 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Jung W, Lee C, Lee D, Na G, Lee D, Choi I, Park S, Seo S, Yang J, Choi JS, Choi JS, et al: The 15-deoxy-δ12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via enhancement of the platelet‑activating factor acetylhydrolase activity in human retinal pigment epithelial cells. Int J Mol Med 33: 449-456, 2014.
APA
Jung, W., Lee, C., Lee, D., Na, G., Lee, D., Choi, I. ... Choi, I. (2014). The 15-deoxy-δ12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via enhancement of the platelet‑activating factor acetylhydrolase activity in human retinal pigment epithelial cells. International Journal of Molecular Medicine, 33, 449-456. https://doi.org/10.3892/ijmm.2013.1588
MLA
Jung, W., Lee, C., Lee, D., Na, G., Lee, D., Choi, I., Park, S., Seo, S., Yang, J., Choi, J. S., Lee, Y., Park, W. S., Choi, I."The 15-deoxy-δ12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via enhancement of the platelet‑activating factor acetylhydrolase activity in human retinal pigment epithelial cells". International Journal of Molecular Medicine 33.2 (2014): 449-456.
Chicago
Jung, W., Lee, C., Lee, D., Na, G., Lee, D., Choi, I., Park, S., Seo, S., Yang, J., Choi, J. S., Lee, Y., Park, W. S., Choi, I."The 15-deoxy-δ12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via enhancement of the platelet‑activating factor acetylhydrolase activity in human retinal pigment epithelial cells". International Journal of Molecular Medicine 33, no. 2 (2014): 449-456. https://doi.org/10.3892/ijmm.2013.1588