Diacylglycerol Kinase ζ Inhibits Ventricular Tachyarrhythmias in a Mouse Model of Heart Failure - Roles of Canonical Transient Receptor Potential (TRPC) Channels
Diacylglycerol Kinase ζ Inhibits Ventricular Tachyarrhythmias in a Mouse Model of Heart Failure - Roles of Canonical Transient Receptor Potential (TRPC) Channels
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DOI：
10.1253/circj.cj-10-1213
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发表时间：
2011-10-01
影响因子：
3.3
通讯作者：
Yamada, Mitsuhiko
中科院分区：
文献类型：
--
作者：
Hirose, Masamichi;Takeishi, Yasuchika;Yamada, Mitsuhiko
背景：在我们的研究中，二酰基甘油激酶ζ（DGKzeta）抑制心力衰竭（HF）小鼠模型的房性快速心律失常。然而，DGKzeta是否能预防HF诱导的室性快速性心律失常（VT）尚不清楚。方法和结果：DGKzeta-对VT的影响使用瞬时心脏表达活化G蛋白（α q）的转基因小鼠（G α（q）-TG; HF模型）和心脏特异性过表达DGK zeta和活化G alpha（q）的双转基因小鼠，（G alpha（q）/DGKzeta-TG）。在G α（q）-TG小鼠中经常观察到室性早搏（PVC）和/或VT，但在G α（q）/DGKzeta-TG和野生型（WT）小鼠中没有观察到（P
Background: Diacylglycerol kinase zeta (DGK zeta) inhibited atrial tachyarrhythmias in a mouse model of heart failure (HF) in our study. However, whether DGK zeta prevents the HF-induced ventricular tachyarrhythmia (VT) is unknown.Methods and Results: Effects of DGK zeta- on VT using transgenic mice with transient cardiac expression of activated G protein (alpha q) (G alpha(q)-TG; model of HF) were elucidated and double transgenic mice with cardiac-specific overexpression of both DGK zeta and the activated G alpha(q) (G alpha(q)/DGK zeta-TG) were used. Premature ventricular contraction (PVC) and/or VT were frequently observed in G alpha(q)-TG mice but not in G alpha(q)/DGK zeta-TG and wild-type (WT) mice (P