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Cadherin-mediated cell adhesion plays a critical role in the maintenance of tissue integrity — not least in heart muscle, in which N-cadherins form part of the intercalated discs that link myocytes.
Misexpression of cadherins could be an important stage in cancer progression, however, since this can increase invasiveness in cancer cell lines. To assess the effects of misexpression of cadherins in vivo, Glenn Radice and co-workers have generated transgenic mice that overexpress N-cadherin or E-cadherin in the heart (see p. 1623). They show that both transgenics develop dilated cardiomyopathy. But the condition is more severe and develops earlier in the mice expressing E-cadherin — a protein not normally present in the adult myocardium. The E-cadherin-expressing mice also exhibit increased levels of cyclin D1 and increased DNA synthesis in cardiomyocytes.
These findings indicate that misexpression of a cadherin subtype can indeed produce abnormal cell behaviour. In this case, it appears to provide an inappropriate growth signal to cardiomyocytes that would otherwise have withdrawn from the cell cycle.
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