RESEARCH ARTICLE
Cell Adhesion Molecule Expression in Human Lens Epithelial Cells After Corticosteroid Exposure
D Celojevic1, T Carlsson2, BR Johansson2, U Nannmark2, A Petersen*, 1
Article Information
Identifiers and Pagination:
Year: 2012Volume: 6
First Page: 42
Last Page: 48
Publisher ID: TOOPHTJ-6-42
DOI: 10.2174/1874364101206010042
Article History:
Received Date: 6/6/2012Revision 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.
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.