Postsynthetic variants of creatine kinase MM.
Postsynthetic variants of creatine kinase MM.
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肌酸激酶 MM 的合成后变体。
DOI：
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发表时间：
1981
期刊：
影响因子：
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通讯作者：
J. Cohn
中科院分区：
文献类型：
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作者：
W. Yasmineh;M. Yamada;J. Cohn
心肌 CK-MM 被发现在 AMI 后发生合成后修饰。通过对正常心脏提取物、AMI 患者的系列血清样本、正常血清和 DMD 患者血清进行等电聚焦研究，发现存在四种变体，分别命名为 MM-I、MM-II、MM-III 和 MM-IV，pH 值分别为 6.90、6.62、6.36 和 6.20。 MM 变体以及两个 MB 变体也可以通过醋酸纤维素电泳来证明。心脏提取物主要含有 MM-I。梗塞后早期（9 至 12 小时）获得的血清样本主要显示 MM-I、MM-II 和 MM-III。随着梗死后时间的增加（24至96小时），逐渐发生转变，其中MM-I和MM-II减少，而MM-III和MM-IV增加。这些结果可以通过将人心脏提取物与正常血清一起孵育增加时间间隔来模拟。正常血清和 DMD 患者血清（两者均含有稳态水平的 MM 同工酶活性）显示出所有四种变异。然而，正常血清中以 MM-I 和 MM-II 为主，而 DMD 患者的血清则以 MM-II 和 MM-III 为主。我们的结论是，AMI 后的合成后修饰过程可能始于心肌损伤部位，因为这些变异可在梗塞后数小时内在血清中得到证实。当酶从损伤部位释放停止后，循环中会发生进一步的改变。这些数据表明，CK 变异的分析可能提供评估 AMI 坏死发作时间的独特方法，并且可能具有检测再梗死和监测损伤部位酶释放持续时间的潜力。
MYocardial CK-MM has been found to undergo postsynthetic modification after AMI. Studies by isoelectric focusing of normal heart extracts, serial serum samples from patients with AMI, normal sera, and sera from patients with DMD revealed the presence of four variants, designated MM-I, MM-II, MM-III and MM-IV, at pH values 6.90, 6.62, 6.36, and 6.20, respectively. The MM variants, together with two MB variants, could also be demonstrated by electrophoresis on cellulose acetate. Heart extract contained primarily MM-I. Serum samples obtained early after infarction (9 to 12 hr) showed predominantly MM-I, MM-II, and MM-III. With increase in time after infarction (24 to 96 hr), there was a gradual shift in which MM-I and MM-II decreased while MM-III and MM-IV increased. These results could be mimicked by incubating an extract of human heart with normal serum for increasing time intervals. Normal serum and serum from DMD patients--both of which contain steady-state levels of MM isoenzyme activity--showed all four variants. There was, however, a preponderance of MM-I and MM-II in normal serum, whereas serum from DMD patients showed a preponderance of MM-II and MM-III. We conclude that the process of postsynthetic modification after AMI probably starts at the site of injury in the myocardium because the variants can be demonstrated in the serum within a few hours after infarction. Further modification then occurs in the circulation after enzyme release from the site of injury has ceased. These data suggest that analysis of CK variants may provide a unique means of assessing the time of onset of necrosis in AMI and may have potential for detecting reinfarction and for monitoring the duration of enzyme release from the site of injury.