Protein 4.1 family and ion channel proteins interact to regulate the process of heart failure in rats
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Updated: Oct 28, 2025

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry
Published on: September 28, 2016
Shuwei Ning1, Lei Hua1, Zhenyu Ji2
1Zhengzhou Key Laboratory, Zhengzhou No. 7 People's Hospital, Zhengzhou, 450016, China.
Insights
The protein 4.1 family interacts with ion channels in heart failure (HF). These interactions suggest 4.1 proteins could be a new therapeutic target for preventing HF progression.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Cytoskeleton Dynamics
Background:
- Heart failure (HF) is a leading cause of death globally, with poorly understood molecular mechanisms.
- The myocardial cytoskeleton is crucial in heart disease, but the role of the protein 4.1 family in HF pathogenesis is unclear.
Purpose of the Study:
- To investigate the expression, localization, and interactions of the protein 4.1 family with ion channels in a rat model of doxorubicin-induced heart failure.
- To explore the potential role of protein 4.1 family members in the development of heart failure.
Main Methods:
- Doxorubicin-induced rat model of heart failure.
- Detection of protein 4.1 family members (4.1R, 4.1G, 4.1N) and ion channel proteins (Nav1.5, SERCA2a, Cav1.2) expression and localization.
- Analysis of protein-protein interactions and co-localization.
Main Results:
- Heart failure group showed increased protein 4.1R and decreased protein 4.1G and 4.1N levels compared to controls.
- Nav1.5 levels increased, while SERCA2a and Cav1.2 levels decreased in the heart failure group.
- Specific interactions and co-localization were observed between protein 4.1R/Nav1.5, 4.1G/SERCA2a, and 4.1N/Cav1.2.
Conclusions:
- The protein 4.1 family is implicated in heart failure development through interactions with key ion channel proteins.
- Protein 4.1 family members represent potential novel therapeutic targets for heart failure treatment.
Abstract:
Heart failure (HF) is a major cause of death in cardiovascular diseases worldwide, and its molecular mechanisms and effective prevention strategies remain to be further studied. The myocardial cytoskeleton plays a pivotal role in many heart diseases. However, little is known about the function of the membrane cytoskeleton 4.1 protein family and related regulatory mechanisms in the pathogenesis of HF. In this study, we detected the localization and expression of the protein 4.1 family and ion channel proteins in a rat HF model induced by doxorubicin (DOX), and studied the interactions between them. Our results showed that compared with the control group, the HF group displayed an increased expression level of protein 4.1R and decreased levels of protein 4.1 G and 4.1 N. The Nav1.5 protein levels were significantly increased, while the SERCA2a and Cav1.2 protein levels were significantly decreased in the HF group. Furthermore, there is co-localization and interaction between protein 4.1R and Nav1.5, protein 4.1 G and SERCA2a, protein 4.1 N and Cav1.2, respectively. Taken together, the results indicated that the protein 4.1 family might be involved in the occurrence and development of HF through its interaction with ion channel proteins, suggesting that 4.1 proteins may serve as a novel therapeutic target for HF.
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