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Cell Adhesion Molecule Expression in Human Lens Epithelial Cells After Corticosteroid Exposure
AIM: The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells (HLEC) subjected to glucocorticoids. METHODS: Human lens epithelial cells were exposed to different concentrations of dexamethasone for 24 hours. Cell adhesion molecule expression...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bentham Open
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386511/ https://www.ncbi.nlm.nih.gov/pubmed/22754600 http://dx.doi.org/10.2174/1874364101206010042 |
Sumario: | AIM: The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells (HLEC) subjected to glucocorticoids. METHODS: Human lens epithelial cells were exposed to different concentrations of dexamethasone for 24 hours. Cell adhesion molecule expression was studied by western blot and immunohistochemistry of vimentin, N-cadherin, E-cadherin, α-catenin, β-catenin and γ-catenin. Expression of the glucocorticoid receptor (GR) was also studied. Cell morphology was examined by transmission electron microscopy (TEM). RESULT: Expression of N-cadherin, α-catenin, β-catenin and GR was significantly decreased in dexamethasone exposed cells as compared to unexposed cells. No significant change in γ-catenin was present. Visualization of adhesion molecules, N-cadherin and α-catenin, by immunohistochemistry showed decreased antigen reactivity in dexamethasone exposed as compared to the unexposed cells. However, no change was seen for β-catenin and γ-catenin. E-cadherin was not detectable using western blot or immunohistochemistry. TEM showed multilayering of cells, vacuole formation and appearance of electron-dense multivesicular bodies in HLEC exposed to 0, 0.1, 1, 10 and 100 αM dexamethasone. CONCLUSION: Glucocorticoids affect several adhesion molecules in lens epithelial cells, something that may contribute to the pathogenesis of posterior subcapsular opacification. |
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