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Cell adhesion molecule expression in human lens epithelial cells after corticosteroid exposure
D Celojevic1, T Carlsson, Br Johansson
1Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation/Ophthalmology.
The Open Ophthalmology Journal
|July 4, 2012
Summary
Glucocorticoids significantly decrease cell adhesion molecules like N-cadherin and catenins in human lens epithelial cells (HLEC). This molecular change may contribute to posterior subcapsular opacification development.
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Biology
Background:
- Cell adhesion molecules are crucial for maintaining ocular tissue structure.
- Glucocorticoids are commonly used in ophthalmology but can have side effects.
- Posterior subcapsular opacification is a known complication of corticosteroid use.
Purpose of the Study:
- To investigate the impact of glucocorticoids on cell adhesion molecule expression in human lens epithelial cells (HLEC).
- To explore the potential role of altered cell adhesion in glucocorticoid-induced ocular pathologies.
Main Methods:
- HLEC were treated with varying concentrations of dexamethasone.
- Western blot and immunohistochemistry were used to analyze expression of N-cadherin, E-cadherin, α-catenin, β-catenin, and γ-catenin.
- Glucocorticoid receptor (GR) expression and cell morphology via transmission electron microscopy (TEM) were also assessed.
Main Results:
- Dexamethasone treatment significantly reduced the expression of N-cadherin, α-catenin, and β-catenin, as well as GR.
- Immunohistochemistry confirmed reduced N-cadherin and α-catenin antigenicity.
- TEM revealed cellular changes including multilayering and vacuole formation in treated HLEC.
Conclusions:
- Glucocorticoids alter the expression of key cell adhesion molecules in HLEC.
- These alterations in cell adhesion may play a role in the pathogenesis of posterior subcapsular opacification.
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