Abstract
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.
Highlights
Glucocorticoid-induced cataract is a common clinical condition
Glucocorticoids affect several adhesion molecules in lens epithelial cells, something that may contribute to the pathogenesis of posterior subcapsular opacification
In a previous study from our group, we found an increase in proliferation as well as the apoptosis in native human lens epithelial cells after exposure to dexamethasone
Summary
Glucocorticoid-induced cataract is a common clinical condition. the association between topical and systemic steroid use and increased occurrence of posterior subcapsular cataract (PSC) has been known since 1960 [1], the mechanism behind this type of lens opacification has yet not been elucidated. Several mechanisms such as osmotic failure [2, 3], metabolic disturbances [3], protein adduct formation [3,4,5,6], conformational changes due to oxidative stress [3, 6,7,8], and receptor mediated changes [3, 6, 8,9,10,11] have been proposed to account for PSC formation, but the results are inconclusive. Adherens junctions are protein complexes that form strong cell-cell contacts between adjacent cells. The classical view is that adherens junctions mediate adhesion between cells by linking the cytoplasmic tail of the calcium-
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