Nakao K, Yasue H, Fujimoto K, Jougasaki M, Yamamoto H, Hitoshi Y, Takatsu K, Miyamoto E
Division of Cardiology, Kumamoto University School of Medicine, Japan.
Circulation. 1992 Dec;86(6):1727-37. doi: 10.1161/01.cir.86.6.1727.
This study was designed to examine the expression of atrial/fetal-type myosin light chain 1 (ALC1) in human ventricles with old myocardial infarction and in control hearts.
The expression of immunoreactive (ir) ALC1 was examined in the subendocardial and subepicardial myocardium of the infarcted and the noninfarcted regions in the left ventricles with old myocardial infarction (n = 12) and of the control left ventricles (n = 8). For the analysis, we prepared two monoclonal antibodies, KA1 and KB1, that were specific for only ALC1 and for both ALC1 and ventricular myosin light chain 1 (VLC1), respectively. The ir-ALC1 expression ratio [ALC1/(ALC1 + VLC1), %] of the subendocardial myocardium, determined densitometrically by Western blotting with KB1, was significantly higher in the infarcted region (11.4 +/- 7.3%) than in the noninfarcted region (4.7 +/- 2.3%, p < 0.001) and the control ventricle (1.0 +/- 1.5%, p < 0.0001). In the infarcted region, the subendocardial myocardium contained a significantly greater percentage of ir-ALC1 than the subepicardial myocardium (5.8 +/- 6.7%, p < 0.005). The ir-ALC1 expression ratio had a significant negative correlation with the value of tissue protein concentration (milligrams protein per gram wet weight). The immunohistochemical study with KA1 revealed that the surviving myocytes included in the infarcted region, especially in the ventricular aneurysm, expressed ir-ALC1 strongly in comparison with those in the noninfarcted or the control ventricles.
These results demonstrate increased expression of ALC1 and the regional differences in the failing left ventricles with old myocardial infarction. We conclude that the reexpression of ALC1 in infarcted ventricles occurs as one of the regional responses to increased load and may be a useful biochemical marker for the appearance of fetal-type myocytes.
本研究旨在检测心房/胎儿型肌球蛋白轻链1（ALC1）在陈旧性心肌梗死患者心室及对照心脏中的表达情况。
检测了12例陈旧性心肌梗死患者左心室梗死区和非梗死区以及8例对照左心室的心内膜下和心外膜下心肌中免疫反应性（ir）ALC1的表达。为进行分析，我们制备了两种单克隆抗体，KA1和KB1，它们分别仅对ALC1以及对ALC1和心室肌球蛋白轻链1（VLC1）具有特异性。通过用KB1进行蛋白质印迹法密度测定的心内膜下心肌的ir-ALC1表达率[ALC1/(ALC1 + VLC1)，%]，在梗死区（11.4±7.3%）显著高于非梗死区（4.7±2.3%，p<0.001）和对照心室（1.0±1.5%，p<0.0001）。在梗死区，心内膜下心肌中ir-ALC1的百分比显著高于心外膜下心肌（5.8±6.7%，p<0.005）。ir-ALC1表达率与组织蛋白浓度值（每克湿重毫克蛋白）呈显著负相关。用KA1进行的免疫组织化学研究显示，梗死区存活的心肌细胞，尤其是室壁瘤中的心肌细胞，与非梗死或对照心室中的心肌细胞相比，ir-ALC1表达强烈。
这些结果表明陈旧性心肌梗死导致左心室功能衰竭时ALC1表达增加及区域差异。我们得出结论，梗死心室中ALC1的重新表达是对负荷增加的区域反应之一，并可能是胎儿型心肌细胞出现的有用生化标志物。
