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Remodeling the intercalated disc leads to cardiomyopathy in mice misexpressing cadherins in the heart. Paper-9249315. Ectopic expression of cadherins is associated with changes in tumor cell behavior and pathology.
Both N- and E-cadherin transgenic animals developed dilated cardiomyopathy. Paper-9249315.
However, misexpression of E-cadherin led to earlier onset and increased mortality compared with N-cadherin mice. Paper-9249315.
E-cadherin was localized to the intercalated disc structure in these animals similar to endogenous N-cadherin. Paper-9249315.
A dramatic decrease in connexin 43 was associated with the hypertrophic response in E-cadherin transgenic mice. Paper-9249315.
The cadherin family of cell adhesion receptors, located in the adherens junction, interact homophilically to mediate strong cell-cell adhesion. Paper-9249315.
The contractile force of the cardiomyocyte is transmitted through the adherens junction, a component of the intercalated disc, enabling the myocardium to function as a syncytium.
By contrast, N-cadherin overexpressing transgenic mice did not exhibit an increase in cyclin D1, suggesting that E-cadherin may provide a specific growth signal to the myocyte. Paper-9249315.
Myofibril organization appeared normal although, vinculin, which normally localizes to the intercalated disc, was redistributed to the cytoplasm in the E-cadherin transgenic mice. Paper-9249315.
Furthermore, E-cadherin induced cyclin D1, nuclear reduplication, and karyokinesis in the absence of cytokinesis, resulting in myocytes with two closely opposed nuclei. Paper-9249315.
To examine the effect of cadherin specificity on cardiac structure and function, we expressed either the epithelial cadherin, E-cadherin, or N-cadherin in the heart of transgenic mice. Paper-9249315.
This study demonstrates that modulation of cadherin- mediated adhesion can lead to dilated cardiomyopathy and that E-cadherin can stimulate DNA replication in myocytes normally withdrawn from the cell cycle. Paper-9249315.
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iHOP - Information Hyperlinked over Proteins .
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