Opposing effects of δ and εPKC in ethanol-induced cardioprotection
Opposing effects of δ and εPKC in ethanol-induced cardioprotection
复制标题
DOI：
10.1006/jmcc.2000.1330
复制
发表时间：
2001-03-01
影响因子：
5
通讯作者：
Mochly-Rosen, D
中科院分区：
文献类型：
--
作者：
Chen, CH;Mochly-Rosen, D
少量乙醇可减少缺血引起的心脏损伤。分离的心肌细胞和完整心脏中急性暴露于少量乙醇可防止缺血性损伤，这归因于蛋白激酶 C (PKC) 的激活。我们之前发现两种 PKC 同工酶，δ 和 epsilon，在几种细胞模型中被乙醇激活。在这里，我们灌注了在完整心脏中生成的同工酶选择性激动剂和拮抗剂肽，以确定这两种同工酶在乙醇诱导的短暂性缺血保护中的作用。乙醇诱导的保护需要 epsilon PKC 激活，而 delta PKC 激活会导致进一步的损害。这些数据解释了关于急性接触乙醇在预防心脏缺血方面的作用的相互矛盾的报告。还讨论了这些发现的临床意义，(C) 2001 学术出版社。
Low amounts of ethanol reduce cardiac damage induced by ischemia. The protection from ischemic damage by acute exposure to low amounts of ethanol in isolated myocytes and intact heart have been attributed to activation of protein kinase C (PKC). We previously found that two PKC isozymes, delta and epsilon, are activated by ethanol in several cell models, Here, we perfused isozyme selective agonist and antagonist peptides that rue have generated into intact heart to determine the role of these two isozymes in ethanol-induced protection from transient ischemia. Whereas epsilon PKC activation was required for ethanol-induced protection, delta PKC activation led to Further damage. These data explain the conflicting reports on the role of acute exposure to ethanol in protection from cardiac ischemia. The clinical implications of these findings are also discussed, (C) 2001 Academic Press.