Effects of cadmium on E-cadherin and VE-cadherin in mouse lung.

Exposure to Cd(2+) via inhalation or intratracheal instillation results in pulmonary edema, which is followed by the influx of leukocytes, the proliferation of type II pneumocytes and eventual scarring and fibrotic changes. While the general toxic effects of Cd(2+) in the lung have been well characterized, the specific molecular mechanisms underlying these effects have yet to be elucidated. Previously we have shown that Cd(2+) can disrupt the adhering junctions between various types of epithelial and endothelial cells in culture, most likely by perturbing the function of the Ca(2+) dependent cell adhesion molecules E-cadherin and VE-cadherin respectively.

Chlamydia trachomatis disrupts N-cadherin-dependent cell-cell junctions and sequesters beta-catenin in human cervical epithelial cells.

The cadherin/catenin complex serves as an important structural component of adherens junctions in epithelial cells. Under certain conditions, beta-catenin can be released from this complex and interact with transcription factors in the nucleus to stimulate the expression of genes that regulate apoptosis and cell cycle control. While studying the effects of the bacterial pathogen Chlamydia trachomatis on human cervical epithelial cells in culture, we observed that C.