STRESS PROTEIN 60 DURING MYOCARDIAL ISCHEMIA

冠状动脉疾病可导致慢性心力衰竭，需要 血运重建(旁路手术)或危及生命的心脏 心律不齐。它是150万急性心肌梗死的原因 在美国，每年有超过一半的脑梗塞是致命的。它的成本 是美国目前所有医学疾病中最高的。冠状动脉 动脉疾病影响心肌(心肌)的血液供应 因此，减少了对心肌细胞的氧气输送。这个 心肌细胞线粒体是心肌缺血的主要靶点之一。 诱导性损害。氧输送的限制减少了线粒体 氧化磷酸化，有助于减少 细胞内三磷酸腺苷水平。一些调查人员表示， 线粒体在修复后不能自我修复 血液流动可能是导致最终死亡的关键事件之一 心肌细胞。尽管目前还不清楚肌膜或 线粒体损伤是心肌细胞不可逆性损伤的主要事件。 心肌细胞线粒体改变在心肌细胞减少中的作用 功能不会受到质疑。最近的研究表明，热休克 蛋白(HSP)60，是应激蛋白家族的成员，是 被认为在氧化应激过程中具有保护作用，是 线粒体内多聚体酶复合体的组装。我们 最近发现，在急性冠状动脉降支闭塞期间 在大鼠心脏中动脉注射30分钟，导致心脏缺血 左心室HSP60mRNA有明显的、特异性的增加 水平。这一发现使我们相信HSP60和其他相关的HSP一样 可能起到保护作用，并可能参与修复 线粒体酶复合体对细胞的正常功能至关重要 线粒体。我们的目标是研究这种由缺血引起的 热休克蛋白60表达的变化及热休克蛋白60是否参与保护 线粒体中有助于脑缺血恢复的过程 心肌细胞的损伤。

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.