STRESS PROTEIN 60 DURING MYOCARDIAL ISCHEMIA

冠状动脉疾病可导致慢性心力衰竭， 血运重建（旁路手术）或危及生命的心脏 心律不齐它是导致150万急性心肌梗死的原因 在美国，每年有1000例脑梗死，其中一半以上是致命的。其成本 是目前全国所有医学疾病中最高的。冠状 动脉疾病影响心肌的血液供应 因此减少了向心肌细胞的氧输送。的 心肌细胞的线粒体是缺血的主要靶点之一， 诱发的损害。氧气输送的限制减少了线粒体 氧化磷酸化，并有助于减少 细胞内ATP水平。一些调查人员指出， 线粒体不能自我修复， 血液流动可能是导致最终死亡的关键事件之一 心肌细胞。尽管尚不清楚肌膜或 线粒体损伤是不可逆损伤的主要事件， 心肌细胞线粒体改变在心肌细胞凋亡中的作用 功能没有问题。最近的研究表明，热休克 蛋白（HSP）60，它是应激蛋白家族的成员， 被认为在氧化应激期间具有保护作用， 线粒体内多聚体酶复合物的组装。我们 最近发现，在冠状动脉降支急性闭塞期间， 动脉30分钟，这导致缺血，在大鼠心脏 左室心肌HSP60 mRNA表达明显增加 水平这一发现使我们相信，HSP60作为其他相关的HSP， 可能具有保护作用，并可能参与修复 线粒体酶复合物对细胞的正常功能至关重要， 线粒体我们的目的是研究这种缺血诱导的 HSP60表达的变化，并确定HSP60是否介导保护作用 线粒体中有助于从缺血恢复的过程 心肌细胞损伤。

Coronary artery disease can lead to chronic heart failure, need for revascularization (by-pass surgery), or life-threatening cardiac arrhythmias. It is the cause of one and a half million acute myocardial infarctions per year in the USA, more than half of them lethal. Its cost is the highest of all Current medical diseases in the nation. Coronary artery disease affects the blood supply of the heart muscle (myocardium) and, therefore, decreases oxygen delivery to myocardial cells. The mitochondria of cardiac myocytes is one of the major targets for ischemia- induced damage. Limitations of oxygen delivery reduces mitochondrial oxidative phosphorylation and contributes to the reduction of intracellular ATP levels. Some investigators have indicated that the inability of the mitochondria to self-repair following restoration of blood flow may be one of the crucial events leading to the ultimate death of myocardial cells. Although it is not clear if sarcolemmal or mitochondrial damage is the main event in the irreversible damage of the myocardial cell, the role of mitochondrial changes in decreased myocardial functions are not questioned. Recent studies have shown that heat shock protein (HSP) 60, which is a member of the stress protein family and are thought to have a protective role during oxidative stress, is required for the assembly of multimeric enzyme complexes within the mitochondria. We have recently found that during acute occlusion of the descending coronary artery for 30 minutes in the rat heart, which leads to ischemia in the left ventricle, there is a marked and specific increase in HSP6O mRNA level. This finding leads us to believe that HSP6O as other related HSPs may have a protective role and is probably involved in the repair of the mitochondrial enzymatic complexes vital for the normal function of the mitochondria. It is our objective to investigate this ischemia-induced change in HSP6O expression and determine if HSP60 mediates protection processes in the mitochondria that contribute to recovery from ischemic injury in the myocardial cell.