Kir2.3 knock-down decreases IK1 current in neonatal rat cardiomyocytes

FEBS Lett. 2008 Jun 25;582(15):2338-42. doi: 10.1016/j.febslet.2008.05.023. Epub 2008 May 27.

Abstract

Inward rectifier potassium Kir2.x channels mediate cardiac inward rectifier potassium currents (I(K1)). As a subunit of Kir2.x, the physiological role of Kir2.3 in native cardiomyocytes has not been reported. This study shows that Kir2.3 knock-down remarkably down-regulates Kir2.3 expression (Kir2.3 protein was reduced to 19.91+/-3.24% on the 2nd or 3rd day) and I(K1) current densities (at -120 mV, control vs. knock-down: -5.03+/-0.24 pA/pF, n=5 vs. -1.16+/-0.19 pA/pF, n=7, P<0.001) in neonatal rat cardiomyocytes. The data suggest that Kir2.3 plays a potentially important role in I(K1) currents in neonatal rat cardiomyocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Gene Expression
  • Membrane Potentials* / genetics
  • Microscopy, Confocal
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / physiology*
  • Patch-Clamp Techniques
  • Potassium Channels, Inwardly Rectifying / genetics
  • Potassium Channels, Inwardly Rectifying / physiology*
  • RNA Interference
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Kcnj4 protein, rat
  • Potassium Channels, Inwardly Rectifying