Modulation of Cadherin and Catenins Expression by Tumor Necrosis Factor- α and Dexamethasone in Human Bronchial Epithelial Cells


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Abstract

Asthma is an inflammatory disease, and the epithelial mesenchymal unit appears to be of importance in regulating the disease mechanisms. Cell-cell adhesion plays an important role in tissue morphogenesis and homeostasis and is commonly mediated by cadherins, a family of Ca2 +-dependent transmembrane adhesion receptors. The cadherin family is involved in control of the cellular architecture. Proinflammatory cytokines such as tumor necrosis factor (TNF)- α are involved in asthma and may interfere with epithelial integrity. In the present study, we investigated the role of TNF- α and dexamethasone on the expression of E-cadherin, β -catenin, and γ -catenin. We used two bronchial epithelial cell models: primary small airway epithelial cell cultures and primary culture obtained from human bronchial tubes. After 48 h of TNF- α stimulation with or without dexamethasone expression of E-cadherin, β -catenin and γ -catenin were analyzed using Western blot analysis and immunofluorescence. This study showed a decrease in the expression of adhesion molecules in both epithelial cell cultures after stimulation. Dexamethasone and anti-TNF- α inhibited this effect. In unstimulated cells, E-cadherin and β - and γ -catenin expression was membranous, expressed only on the lateral cell wall with minimal cytoplasmic expression. Immunoreactivity was cytoplasmic in stimulated cells. We demonstrated, using Western blot analysis and immunofluorescence, that proinflammatory cytokines could be responsible for structural damage to the epithelium and that this process was potentially reversed by steroids.

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