He Yusong, Pan Qin, Li Jun, Chen Huaizhi, Zhou Qinshu, Hong Kui, Brugada Ramon, Perez Guillermo J, Brugada Pedro, Chen Yi-Han
Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China.
FEBS Lett. 2008 Jun 25;582(15):2338-42. doi: 10.1016/j.febslet.2008.05.023. Epub 2008 May 27.
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.
内向整流钾通道Kir2.x介导心脏内向整流钾电流（I(K1)）。作为Kir2.x的一个亚基，Kir2.3在天然心肌细胞中的生理作用尚未见报道。本研究表明，敲低Kir2.3可显著下调Kir2.3的表达（在第2天或第3天，Kir2.3蛋白降至19.91±3.24%）以及新生大鼠心肌细胞中的I(K1)电流密度（在-120 mV时，对照组与敲低组：-5.03±0.24 pA/pF，n = 5 对比 -1.16±0.19 pA/pF，n = 7，P<0.001）。这些数据表明，Kir2.3在新生大鼠心肌细胞的I(K1)电流中发挥着潜在的重要作用。
