May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Cell Signalling in the Corneal Endothelium
Author Affiliations & Notes
  • G. Chan
    Cell Biology, Inst Ophthalmology, London, United Kingdom
  • F. Larkin
    Moorfields Eye Hospital, London, United Kingdom
  • S.E. Moss
    Moorfields Eye Hospital, London, United Kingdom
  • Footnotes
    Commercial Relationships  G. Chan, None; F. Larkin, None; S.E. Moss, None.
  • Footnotes
    Support  Fight for Sight
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4719. doi:
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      G. Chan, F. Larkin, S.E. Moss; Cell Signalling in the Corneal Endothelium . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4719.

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

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Abstract: : Purpose: The purpose of our investigation is to gain insight into the molecular basis of proliferation and apoptosis in corneal endothelial cells. Since corneal opacity is associated primarily with an age-related decrease in corneal endothelial cell density, it is necessary to understand the basic cell signalling events underlying this phenomenon if we are to develop rational therapeutic strategies. We present the results of studies that explore the relationship between growth factor-elicited signal transduction and extracellular matrix in corneal endothelial cells. Methods:Mouse primary corneal endothelial cells and a mouse corneal endothelial cell line cultured on a range of extracellular matrix proteins were stimulated with various growth factors. Cell signalling proteins activated by growth factor stimulation were identified by western blotting. Results: In the mouse corneal endothelial cell line, both epidermal growth factor (EGF) and fibroblast growth factor-2 (FGF-2) stimulated a peak in ERK activation within 5 minutes of stimulation. However, ERK activation by EGF was markedly less sustained than that elicited by FGF-2. In contrast, primary mouse corneal endothelial cells reacted differently to FGF-2 treatment, showing a biphasic ERK activation. Similar results were obtained regardless of extracellular matrix. Conclusions: ERK activation is different in the mouse corneal endothelial cell line compared to primary mouse corneal endothelial cells. Thus, the endothelial cell line may not be a reliable model in which to study proliferative responses. Nevertheless, differences in the longevity of ERK activation are associated with cellular decisions to either differentiate or proliferate. Future work will address the mitogenic consequences of growth factor stimulation in corneal endothelial cells.

Keywords: cornea: endothelium • growth factors/growth factor receptors • extracellular matrix 

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