Kir2.3 knock-down decreases IK1 current in neonatal rat cardiomyocytes.
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.
He
Yusong
Y
Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China.
Pan
Qin
Q
Li
Jun
J
Chen
Huaizhi
H
Zhou
Qinshu
Q
Hong
Kui
K
Brugada
Ramon
R
Perez
Guillermo J
GJ
Brugada
Pedro
P
Chen
Yi-Han
YH
D000818:Animals; D002478:Cells, Cultured; D015870:Gene Expression; D008564:Membrane Potentials / Q000235:genetics; D018613:Microscopy, Confocal; D032383:Myocytes, Cardiac / Q000166:cytology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics / Q000502:physiology*; D034622:RNA Interference; D051381:Rats; D017207:Rats, Sprague-Dawley
C490968:Kcnj4 protein, rat; D024661:Potassium Channels, Inwardly Rectifying