Melguizo C, Prados J, Velez C, Aránega A E, Marchal J A, Aránega A
Department of Health Sciences and Clinical Psychology, University of Almería, Spain.
Jpn Heart J. 1997 Nov;38(6):779-86. doi: 10.1536/ihj.38.779.
We used one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis of myocardial proteins followed by Western blotting to study the formation of antiheart antibodies during three months after myocardial infarction and the relationship between the appearance of antibodies and clinical and laboratory findings. Fifty-four percent of the 66 patients with infarction had different types of antiheart antibodies. The autoantibodies detected most frequently were against 35 and 42 kDa cardiac proteins. Immunoblottings with purified proteins showed that these autoantibodies reacted against myocardial tropomyosin and actin, which have been detected after acute myocardial infarction and can have immunogenetic activity through a humoral immune response. However, only the presence of autoantibody against myocardial tropomyosin correlated significantly with the presence of clinical and laboratory findings. Our results suggest that autoantibody against myocardial tropomyosin may play an immunopathogenic role in the development of symptoms in these patients.
我们采用心肌蛋白的一维十二烷基硫酸钠-聚丙烯酰胺凝胶电泳,随后进行蛋白质印迹法,以研究心肌梗死后三个月内抗心脏抗体的形成以及抗体出现与临床和实验室检查结果之间的关系。66例梗死患者中有54%出现了不同类型的抗心脏抗体。最常检测到的自身抗体是针对35 kDa和42 kDa心脏蛋白的。用纯化蛋白进行免疫印迹显示,这些自身抗体与心肌原肌球蛋白和肌动蛋白发生反应,急性心肌梗死后已检测到这些蛋白,并且它们可通过体液免疫反应具有免疫遗传活性。然而,只有抗心肌原肌球蛋白自身抗体的存在与临床和实验室检查结果的存在显著相关。我们的结果表明,抗心肌原肌球蛋白自身抗体可能在这些患者症状的发展中起免疫致病作用。