April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Corticosteroids-induced Toxicity And Cell Death Mechanisms In Vascular Endothelial Cells
Author Affiliations & Notes
  • Ikram El-zaoui
    INSERM U 872 Team 17, Paris, France
    Université Paris Descartes, Paris, France
  • Fatemeh Valamanesh
    INSERM U 872 Team 17, Paris, France
    Fondation Ophtalmologique A. De Rothschild, Paris, France
  • Francine F. Behar-Cohen
    INSERM U 872 Team 17, Paris, France
    Hôpital Hotel Dieu, Paris, France
  • Alicia Torriglia
    INSERM U 872 Team 17, Paris, France
    Université Paris Descartes, Paris, France
  • Footnotes
    Commercial Relationships  Ikram El-zaoui, None; Fatemeh Valamanesh, None; Francine F. Behar-Cohen, None; Alicia Torriglia, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4323. doi:
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      Ikram El-zaoui, Fatemeh Valamanesh, Francine F. Behar-Cohen, Alicia Torriglia; Corticosteroids-induced Toxicity And Cell Death Mechanisms In Vascular Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4323.

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

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Purpose: : Glucocorticosteroids have been widely used in the treatment of many diseases. In the eye they are used in the treatment of macular oedema and retinal neo-vascularization, currently associated with diabetic retinopathies. Previous work have shown a toxicity of glucocorticosteroids on several retinal cells, like retinal endothelial cells, Muller cells and Retinal pigmented epithelial cells. In all these cells we have shown that cell death is triggered through non conventional molecular mechanisms, e.g. caspase independent mechanisms. We investigate here the toxicity of these compounds on endothelial cells of the microcirculation.

Methods: : We performed our study on cells of the human microcirculation (HMEC) and bovine retinal endothelial cells (BREC). Four glucocorticosteroids were used : hydrocortisone, dexamethasone, dexamethasone phosphate and triamcinolone acetonide). DL50 for these compounds were evaluated though MTT test. Mechanisms of cells death have been explored using the evaluation of lactate dehydrogenase release, DNA electrophoresis, immunohistochemistry and western blot.

Results: : We found a decrease of cell viability that increases with the degree of hydrophobicity of the glucocorticosteroids. The most hydrophobics been the most toxic. DL50 on HMEC was 0.1 mg/ml for hydrocortisone, dexamethasone and triamcinolone acetonide and it was 0.8mg/ml for dexamethasone phosphate. The cell type is also important. We found that the endothelial cells of the general microcirculation are more sensitive that the retinal endothelial cells. The evaluation of the cell death pathways activated showed that activation of a caspase independent pathway, the LEI/L-DNase II is involved in this cell death.

Conclusions: : At the therapeutically used doses glucocorticosteroids are toxic for endothelial cells. This should be kept in mind in the clinical use of these compounds.

Keywords: corticosteroids • inflammation • apoptosis/cell death 

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