Exp Mol Med.  2004 Aug;36(4):367-371.

Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development

Affiliations
  • 1AK St. Georg Abteilung fur Kardiologie Lohmuhlenstrasse 5 20099 Hamburg, Germany.
  • 2Max Planck Institut fur Medizinische Forschung Abteilung Zellphysiologie Jahnstrasse 29 69120 Heidelberg, Germany.
  • 3Universitatsklinik Heidelberg Innere Medizin III INF410, 69120 Heidelberg, Germany. joerg_zehelein@med.uni-heidelberg.de

Abstract

To understand molecular mechanisms that regulate formation and maintenance of cardiac IKr (rapidly activating component of the delayed rectifier K+ current), we have investigated the spatiotemporal expression pattern of two rat potassium voltage-gated channels, namely subfamily H (eag-related), member2 (KCNH2) (alias name: rERG) and Isk-related family, member2 (KCNE2) (alias name: rMiRP1) during late embryonic development by means of the in situ hybridization technique. KCNE2 is transcribed predominantly in atrial und ventricular myocardium at stages E14.5-E18.5dpc and only a minor signal emerged in the tongue at E16.5dpc. In contrast, KCNH2 transcripts appeared in a less confined pattern with intense signals in atrial and ventricular myocardium, somites, spinal cord, bowel system, central nervous system and thymus at stages E14.5-E18.5dpc. Non-cardiac expression even exceeds the intensity of the cardiac signal, indicating that KCNH2 contributes to K+ currents in non-cardiac tissue as well. Transcription of the rat beta-subunit KCNE2 is present in all regions of the fetal myocardium and co-distributes perfectly with transcription of the pore forming alpha-subunit KCNH2. It seems likely that KCNH2 and KCNE2 are linked to form cardiac IKr channels, associated to cardiogenesis and cardiomyocyte excitability.

Keyword

cardiac development; delayed rectifier; ERG; fetal expression; IKr current; MiRP1
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