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Updated: May 9, 2026

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
Published on: March 12, 2013
Altered expression of genes for Kir ion channels in dilated cardiomyopathy
Viktoria Szuts1, Dalma Ménesi, Zoltán Varga-Orvos
1Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary.
Insights
Gene expression of Kir2.x potassium channels and SAP97 changes in dilated cardiomyopathy (DCM). Healthy hearts show high KCNJ2, KCNJ12, KCNJ4, and low KCNJ14. DCM alters Kir2.1, Kir2.3, Kir2.2, and DLG1 expression.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genetics
Background:
- Dilated cardiomyopathy (DCM) is a complex heart condition affecting the left ventricle.
- Cardiac muscle repolarization involves Kir2.x potassium channels, crucial for electrical stability.
Purpose of the Study:
- To investigate gene expression changes of Kir2.x channels and SAP97 in healthy versus DCM human hearts.
- To understand the molecular basis of electrical and functional alterations in DCM.
Main Methods:
- Analysis of KCNJ gene (encoding Kir2.x channels) and DLG1 (encoding SAP97) expression in human ventricular tissue.
- Comparison of gene expression profiles between healthy and DCM hearts across different age groups.
Main Results:
- In healthy hearts, KCNJ2, KCNJ12, KCNJ4 were highly expressed, while KCNJ14 was low.
- DCM hearts showed upregulated Kir2.1 and Kir2.3, and downregulated Kir2.2 channel expression.
- DLG1/SAP97 expression decreased with age in normal hearts and was significantly reduced in young DCM patients.
Conclusions:
- Altered expression of Kir2.x channels and SAP97 in DCM suggests a role in disease pathophysiology.
- These molecular changes may contribute to the observed electrical and mechanical dysfunction in dilated cardiomyopathy.
Abstract:
Dilated cardiomyopathy (DCM) is a multifactorial disease characterized by left ventricular dilation that is associated with systolic dysfunction and increased action potential duration. The Kir2.x K⁺ channels (encoded by KCNJ genes) regulate the inward rectifier current (IK1) contributing to the final repolarization in cardiac muscle. Here, we describe the transitions in the gene expression profiles of 4 KCNJ genes from healthy or dilated cardiomyopathic human hearts. In the healthy adult ventricles, KCNJ2, KCNJ12, and KCNJ4 (Kir2.1-2.3, respectively) genes were expressed at high levels, while expression of the KCNJ14 (Kir2.4) gene was low. In DCM ventricles, the levels of Kir2.1 and Kir2.3 were upregulated, but those of Kir2.2 channels were downregulated. Additionally, the expression of the DLG1 gene coding for the synapse-associated protein 97 (SAP97) anchoring molecule exhibited a 2-fold decline with increasing age in normal hearts, and it was robustly downregulated in young DCM patients. These adaptations could offer a new aspect for the explanation of the generally observed physiological and molecular alterations found in DCM.
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