Cell Adhesion Molecule Expression in Human Lens Epithelial Cells After Corticosteroid Exposure
D Celojevic1, T Carlsson2, BR Johansson2, U Nannmark2, A Petersen*, 1
Identifiers and Pagination:Year: 2012
First Page: 42
Last Page: 48
Publisher ID: TOOPHTJ-6-42
Article History:Received Date: 6/6/2012
Revision Received Date: 9/6/2012
Acceptance Date: 9/6/2012
Electronic publication date: 21/6/2012
Collection year: 2012
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells (HLEC) subjected to glucocorticoids.
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).
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.
Glucocorticoids affect several adhesion molecules in lens epithelial cells, something that may contribute to the pathogenesis of posterior subcapsular opacification.