AI Article Synopsis
- Beta-catenin is important for cell communication and is linked to heart and blood vessel issues, with little research on its role in heart cell death (apoptosis).
- This study examined how beta-catenin affects apoptosis in heart cells from diabetic rats by using a specific plasmid to increase its levels.
- Results showed that high levels of beta-catenin led to more heart cell death and reduced survival signals, suggesting that changes in Wnt/beta-catenin signaling could lead to heart failure.
Article Abstract
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).
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.5603/CJ.a2016.0087 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!