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首页> 外文期刊>American Journal of Physiology >Alterations to myofibrillar protein function in nonischemic regions of the heart early after myocardial infarction.
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Alterations to myofibrillar protein function in nonischemic regions of the heart early after myocardial infarction.

机译：心肌梗塞后早期心脏非缺血区域的肌原纤维蛋白功能改变。

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摘要

Remote-zone left ventricular dysfunction (LVD) contributes to global reductions in contractile function after localized myocardial infarction (MI). However, the molecular mechanisms underlying this form of LVD are not clear. This study tested the hypothesis that myofibrillar protein function is directly affected in remote-zone LVD early after MI. Cardiac myosin and native thin filaments were purified from mouse myocardium taken from both the nonnecrotic zone adjacent to and the nonischemic zone remote from an infarct induced by 1 h of coronary occlusion followed by 24 h of reperfusion. Thin filament velocities were measured using the in vitro motility assay. Results showed that overall function was significantly reduced in samples from both the adjacent (43 +/- 12% of control, n 7) and remote (53 +/- 8% of control, n proteins (P < 0.05). Myosin from the remote zone propelled control thin filaments at reduced velocities similar to those measured above. In contrast, the Ca(2+) sensitivity of remote-zone thin filaments over control myosin was unchanged from control thin filaments (half-maximal at pCa 6.32 +/- 0.08 and 6.27 +/- 0.06, respectively) but showed a 20% increase in velocity at saturating Ca(2+) that parallels an increase in tropomyosin phosphorylation. Myosin dysfunction may be related to oxidation of cysteines in the myosin heavy chains or carbonylation of myosin binding protein-C. We hypothesize that phosphorylation of tropomyosin may serve a compensatory role, augmenting contraction during periods of oxidative stress when myosin function is compromised.
机译：局部心肌梗死（MI）后，偏远区域左心功能不全（LVD）导致总体收缩功能降低。但是，尚不清楚这种形式的LVD的分子机制。这项研究检验了以下假设，即MI后早期，在远区LVD中肌原纤维蛋白功能直接受到影响。从小鼠心肌中纯化心肌肌球蛋白和天然细丝，该小鼠心肌取自邻近的非坏死区和远离缺血的非缺血区，该区域由1 h冠状动脉闭塞继之以24 h再灌注所致。使用体外运动测定法测量细丝速度。结果表明，相邻蛋白（对照组的43 +/- 12％，n 7）和远端蛋白（对照组的53 +/- 8％，n种蛋白质）的总体功能均显着降低（P <0.05）。远程区域以降低的速度推动了控制细丝，其速度与上述测量的结果相似。相比之下，远程区域细丝对对照肌球蛋白的Ca（2+）敏感性与控制细丝相比保持不变（半最大在pCa 6.32 +/-分别为0.08和6.27 +/- 0.06），但在饱和Ca（2+）时显示出20％的速度增加，与原肌球蛋白磷酸化的增加平行。肌球蛋白功能障碍可能与肌球蛋白重链中的半胱氨酸氧化或Cy的羰基化有关肌球蛋白结合蛋白-C。我们假设原肌球蛋白的磷酸化可能起补偿作用，当肌球蛋白功能受损时，在氧化应激期间会增加收缩。

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