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
1 Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation/Ophthalmology
2 Institute of Biomedicine, Department of Medical Chemistry and Cell Biology, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden


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© Celojevic et al.; Licensee Bentham Open.

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.

* Address correspondence to this author at the Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation/Ophthalmology, PO Box 440, SE-405 30 Gothenburg, Sweden; Tel: +46-31-773 33 94; E-mail: Anne.Petersen@gu.se


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.

Keywords: Human lens epithelial cells, glucocorticoids, opacification, TEM, posterior subcapsular cataract, E-cadherin.