April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Complement stimulates Retinal Pigment Epithelial Cells to undergo Pro-inflammatory Changes as in Early Age-Related Macular Degeneration
Author Affiliations & Notes
  • Katharina Lueck
    Ophthalmology, Ophtha-Lab, Muenster, Germany
  • Susanne Wasmuth
    Ophthalmology, Ophtha-Lab, Muenster, Germany
  • Stephen E. Moss
    Ophthalmology, Cell Biology, UCL London, United Kingdom
  • John Greenwood
    Ophthalmology, Cell Biology, UCL London, United Kingdom
  • Albrecht Lommatzsch
    Ophthalmology, Ophthalmolgy at St. Franziskus Hospital, Muenster, Germany
  • Daniel Pauleikhoff
    Ophthalmology, Ophtha-Lab, Muenster, Germany
    Ophthalmology, Ophthalmolgy at St. Franziskus Hospital, Muenster, Germany
  • Footnotes
    Commercial Relationships  Katharina Lueck, None; Susanne Wasmuth, None; Stephen E. Moss, None; John Greenwood, None; Albrecht Lommatzsch, None; Daniel Pauleikhoff, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2295. doi:https://doi.org/
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      Katharina Lueck, Susanne Wasmuth, Stephen E. Moss, John Greenwood, Albrecht Lommatzsch, Daniel Pauleikhoff; Complement stimulates Retinal Pigment Epithelial Cells to undergo Pro-inflammatory Changes as in Early Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2295. doi: https://doi.org/.

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

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  • Supplements
Abstract

Purpose: : A polymorphism in the complement factor H gene, leading to increased complement activation, is associated with the development of age-related macular degeneration (AMD). We therefore examined the effect of human complement sera (HCS) on retinal pigment epithelial (RPE) cells with respect to pro-inflammatory mediators relevant in early AMD.

Methods: : RPE cells were treated with HCS or heat-inactivated (HI)-HCS as a complement-deficient control. Cells were stained for C5b-9 using immunocytochemistry and immunofluorescence, and cell viability was determined. Interleukin (IL) -6, -8 and monocyte chemoattractant protein-1 (MCP-1) were quantified by ELISA and their expression was determined by RT-PCR. Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and tumour necrosis factor-α (TNF-α) were analysed by western blotting. The intracellular distribution of nuclear factor (NF)-kappaB was investigated by immunofluorescence.

Results: : Concentration-dependent increased staining for C5b-9 was observed after HCS treatment, whereas cell viability decreased. ELISA and RT-PCR analysis revealed increased secretion and expression of IL-6, -8 and MCP-1. Western blot analysis showed a concentration-dependent enhancement in ICAM-1, VCAM-1 and TNF-α in response to HCS, and immunofluorescence staining revealed cytosolic to nuclear translocation of NF-kappaB.

Conclusions: : This study suggests that complement may stimulate RPE cells to create a pro-inflammatory environment via NF-kappaB activation which may support early AMD development.

Keywords: age-related macular degeneration • retinal pigment epithelium • inflammation 
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