April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Upregulation of Cell Migration and Proliferation Through the Action of PI-3 Kinase by IL-1β-Induced FGF-2, the Downstream Target of NF-B, in Corneal Endothelial Cells
Author Affiliations & Notes
  • J. Lee
    Doheny Eye Institute, Los Angeles, California
  • J.-S. Song
    Doheny Eye Institute, Los Angeles, California
    Department of Ophthalmology, Korea University College of Medicine, Seoul, Republic of Korea
  • E. Kay
    Doheny Eye Institute, Los Angeles, California
    Department of Ophthalmology, Keck School of Medicine of University of Southern California, Los Angeles, California
  • Footnotes
    Commercial Relationships  J. Lee, None; J.-S. Song, None; E. Kay, None.
  • Footnotes
    Support  NIH/NEI EY06431 and EY03040, and Research to Prevent Blindness, New York, NY.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1807. doi:
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      J. Lee, J.-S. Song, E. Kay; Upregulation of Cell Migration and Proliferation Through the Action of PI-3 Kinase by IL-1β-Induced FGF-2, the Downstream Target of NF-B, in Corneal Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1807.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Our previous work demonstrated that IL-1β, a major proinflammatory cytokine, induces production of FGF-2 through PI 3-kinase and p38. We further investigated whether the NF-ΚB pathway participates in FGF-2 induction by IL-1β and its effect on cell migration and proliferation in corneal endothelial cells (CECs).

Methods: : Scratch-induced directional migration assay was used to measure migratory rates. Cell proliferation was measured by MTT assay. NF-ΚB activity was measured using transcription assay kit. Pharmacological inhibitors were used to block PI 3-kinase, p38, ERK1/2, or NF-ΚB.

Results: : We investigated whether IL-1β induced cell migration and proliferation. Brief stimulation with IL-1β or culture with conditioned media acquired from IL-1β treated cells induced cell migration and proliferation; however, these inductions were completely blocked by the neutralizing antibody to FGF-2, suggesting the involvement of FGF-2 induced by IL-1β. It was also defined that activation of PI 3-kinase and p38 was involved in cell migration, while cell proliferation was simultaneously stimulated by ERK1/2 and PI 3-kinase. We further investigated whether NF-ΚB participates in the induction pathway of FGF-2 by IL-1β. The NF-ΚB activity induced by IL-1β stimulation was 4-fold that of DMEM-cultured cells. The NF-ΚB activity was completely blocked by inhibition of PI 3-kinase and p38. Blocking of the NF-ΚB pathway by sulfasalazine, a specific NF-ΚB inhibitor, greatly decreased the IL-1β-induced FGF-2 production (63%), indicating that the NF-ΚB pathway activated by IL-1β through PI 3-kinase and p38 is involved in FGF-2 production.

Conclusions: : These findings suggest that CECs utilize NF-ΚB as a major transcription factor to produce FGF-2 by IL-1β stimulation through PI 3-kinase and p38. The IL-1β-induced FGF-2 facilitates cell migration via PI 3-kinase and p38, while it stimulates cell proliferation using PI 3-kinase and ERK1/2 in parallel pathways.

Keywords: signal transduction • cornea: endothelium • cornea: basic science 
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