| Autor: |
Masuelli, Laura, Bei, Roberto, Sacchetti, Pamela, Scappaticci, Ilaria, Francalanci, Paola, Albonici, Loredana, Coletti, Anna, Palumbo, Camilla, Minieri, Marilena, Fiaccavento, Roberta, Carotenuto, Felicia, Fantini, Cristina, Carosella, Luciana, Modesti, Andrea, Di Nardo, Paolo |
| Předmět: |
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| Zdroj: |
Cardiovascular Research; Nov2003, Vol. 60 Issue 2, p376, 12p |
| Abstrakt: |
Objective: To evaluate whether cardiomyocyte membrane structure and cell/extracellular matrix adhesion alterations perturb the cadherin/catenin complex in the hypertrophic cardiomyopathy (HCM). Methods: Hypertrophic cardiomyopathic hamster (UM-X7.1 strain) and human hearts were studied by light and electron microscopy, Northern and Western blot analyses and immunohistochemistry. Results: Intercalated disks are disorganized in both hamster and human cardiomyopathic hearts; β-catenin is increased and accumulated in intercalated disks depriving cardiomyocyte nuclei of fundamental signals. The accumulation of β-catenin is post-translationally regulated by an increased Wnt expression, a simultaneous decrease in glycogen synthase kinase 3β (GSK3β) expression and a different expression pattern of adenomatous polyposis coli (APC) isoforms. Conclusion: The reorganization of cell/cell adhesion in cardiomyopathic hearts is mainly contributed by the cadherin/catenin system, which is differently regulated to sustain cell structural rather than signalling needs causing considerable consequences in the determination of cardiomyocyte phenotype and clinical outcome. The accumulation of β-catenin in intercalated disks could concur to increase myocardial wall stiffness and left ventricular end-diastolic pressure (LVEDP) in hypertrophic cardiomyopathic hamster and human hearts. [Copyright &y& Elsevier] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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