Phospholipase D plays a role in ischemic preconditioning in rabbit heart
Phospholipase D plays a role in ischemic preconditioning in rabbit heart
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DOI：
10.1161/01.cir.94.7.1713
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发表时间：
1996-10-01
期刊：
影响因子：
37.8
通讯作者：
Downey, JM
中科院分区：
文献类型：
--
作者：
Cohen, MV;Liu, YG;Downey, JM
背景 蛋白激酶 C (PKC) 的激活被认为是缺血预处理的关键步骤。许多受体激动剂通过刺激磷脂酶 C (PLC) 来激活 PKC，后者将膜磷脂降解为二酰基甘油 (DAG)，这是一种重要的 PKC 辅助因子。然而，腺苷受体（原型预处理途径的关键组成部分）不被认为与心肌细胞中的 PLC 偶联。因此，我们测试了缺血预处理或腺苷是否可能激活磷脂酶 D (PLD) 来产生 DAG。方法和结果 在离体兔心脏中测量 PLD 活性。在离体兔心脏或分散的肌细胞中评估缺血性损伤。 PLD活性从对照水平74.8+/-10.0翻倍至140.0+/-11.5μmol。分钟(-1) 。克(-1) (P
Background Activation of protein kinase C (PKC) is thought to be a critical step in ischemic preconditioning. Many receptor agonists activate PKC via stimulation of phospholipase C (PLC), which degrades membrane phospholipids to diacylglycerol (DAG), an important PKC cofactor. However, adenosine receptors, critical components of the prototypical preconditioning pathway, are not thought to couple to PLC in the cardiomyocyte. We therefore tested whether ischemic preconditioning or adenosine might instead activate phospholipase D (PLD) to produce DAG.Methods and Results PLD activity was measured in isolated rabbit hearts. Ischemic injury was evaluated in either isolated rabbit hearts' or dispersed myocytes. PLD activity doubled from a control level of 74.8+/-10.0 to 140.0+/-11.5 mu mol . min(-1) . g(-1) (P