Altered expression of genes for kir ion channels in dilated cardiomyopathy

Viktoria Szuts, Dalma Ménesi, Zoltán Varga-Orvos, Ágnes Zvara, Nazanin Houshmand, Miklós Bitay, Gábor Bogáts, László Virág, István Baczkó, Balázs Szalontai, Amir Geramipoor, Diego Cotella, Erich Wettwer, Ursula Ravens, Ferenc Deák, László G. Puskás, Julius Gy Papp, Ibolya Kiss, András Varró, Norbert Jost

Research output: Contribution to journalArticle

17 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)648-656
Number of pages9
JournalCanadian journal of physiology and pharmacology
Volume91
Issue number8
DOIs
Publication statusPublished - Aug 1 2013

Keywords

  • Dilated cardiomyopathy
  • I
  • Inward rectifier potassium channels
  • Kir2.x
  • SAP97

ASJC Scopus subject areas

  • Physiology
  • Pharmacology
  • Physiology (medical)

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