Key result
Beta-catenin overexpression in cardiomyocytes induces dose-dependent apoptosis and upregulates fibrosis markers.
Overexpression of beta-catenin in cardiomyocytes promotes apoptosis and fibrosis while suppressing survival proteins, suggesting altered Wnt/beta-catenin signaling may contribute to heart failure pathogenesis.
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May implicate Wnt/beta-catenin in heart failure pathogenesis; leaves open therapeutic targeting in patients.
BACKGROUND: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. METHODS: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. RESULTS: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. CONCLUSIONS: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure. (Cardiol J 2017; 24, 2: 195-205).
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Lin et al. (2016) studied Cardiomyocyte apoptosis. pCMV-b-catenin plasmid was evaluated on Apoptosis and expression of survival and fibrosis markers. Overexpression of beta-catenin in cardiomyocytes induced apoptosis, reduced survival pathway markers, and upregulated fibrosis protein markers in a dose-dependent manner.
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