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Published on: October 26, 2017
Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model
Shaoyan Liu1, Yang Lan1, Yun Zhao2
1Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Insights
Researchers developed a new mouse model to track Connexin 43 (Cx43) protein in vivo. This tool aids in understanding heart failure development and improving cardiac function assessment.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genetic Engineering
Background:
- Heart failure (HF) is a critical condition with high mortality, often stemming from aortic valve stenosis (AVS).
- AVS leads to increased left ventricular load, hypertrophy, and eventual dysfunction, contributing to HF.
- Early assessment of cardiomyopathy and timely intervention are crucial for managing HF progression.
Purpose of the Study:
- To establish a novel genetic tool for in vivo visualization and analysis of Connexin 43 (Cx43) protein.
- To investigate the role of Cx43 in the context of Wnt signaling and myocardial adaptation to aortic valve stenosis.
- To provide a method for assessing Cx43 distribution and its impact on cardiac electrical conduction during disease.
Main Methods:
- Development of a Cx43-BFP-GFP double-reporter mouse model.
- Utilized Cre-loxp recombination system for conditional gene expression and labeling.
- Employed the reporter system to determine Cx43 area, spatial distribution, and functional status in vivo.
Main Results:
- Successfully generated a Cx43-BFP-GFP mouse model for specific in vivo Cx43 labeling.
- The model allows for detailed analysis of Cx43 distribution and changes in cardiac cells.
- Demonstrated the utility of the model in assessing alterations in electrical conduction related to Cx43 status.
Conclusions:
- The Cx43-BFP-GFP mouse model is a valuable genetic tool for studying Cx43 dynamics in cardiovascular disease.
- Understanding Cx43 distribution is key to comprehending HF development and progression.
- This model can facilitate research into improving cardiac function and preventing HF.
Abstract:
Heart failure (HF) is the end stage of various cardiovascular diseases, with high morbidity and mortality, and is associated with a poor prognosis. One of the primary causes of HF is aortic valve disease, manifested by progressive aortic valve stenosis (AVS), resulting in increased left ventricular load, ventricular hypertrophy, ultimately ventricular dysfunction, and HF. Early assessment of the degree of cardiomyopathy and timely intervention is expected to improve patients' cardiac function and delay or even avoid the occurrence of HF. The Wnt signaling pathway is mainly involved in regulating myocardial insufficiency after valve stenosis. Connexin 43 protein (Cx43) is an essential target of Wnt signaling pathway that forms gap junction (GJ) structures and is widely distributed in various organs and tissues, especially in the heart. The distribution and transformation of Cx43 among cardiac cells are crucial for the development of HF. To specifically label Cx43 in vivo, we established a new Cx43-BFP-GFP mouse model with two loxp sites on both sides of the tag BFP-polyA box, which can be removed by Cre recombination. This double-reporter line endowed us with a powerful genetic tool for determining the area, spatial distribution, and functional status of Cx43. It also indicated changes in electrical conduction between cells in a steady or diseased state.
