Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 91, Issue 8, Pages 648-656Publisher
CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/cjpp-2012-0413
Keywords
inward rectifier potassium channels; I-K1; dilated cardiomyopathy; Kir2.x; SAP97
Categories
Funding
- Hungarian Scientific Research Fund [OTKA CNK-77855, K-82079, K-75818, NK-104331]
- National Office for Research and Technology [NKFP_07_01-RYT07_AF, REG-DA-09-2-2009-0115-NCXINHIB]
- National Development Agency
- European Regional Fund [TAMOP-4.2.2-08/1-2008-0013, TAMOP-4.2.1/B-09/1/KONV-2010-0005, TAMOP-4.2.2/B-10/1-2010-0012]
- Hungarian Academy of Sciences
- Hungary-Romania Cross-Border Co-operation Programme (HU-RO_TRANS-MED and HU-RO_CARDIOPOL projects)
- German-Hungarian Research Cooperation DFG [436 UNG 113/176/0-1]
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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 (I-K1) 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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