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心肌病中心肌肌球蛋白同工酶的分布:免疫组织化学和基因分析

Distribution of cardiac myosin isozymes in cardiomyopathy: immunohistochemical and gene analysis.

作者信息

Yazaki Y, Tsuchimochi H, Kurabayashi M, Kawana M, Kimata S

机构信息

Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Jpn Circ J. 1987 Jun;51(6):676-81. doi: 10.1253/jcj.51.676.

DOI:10.1253/jcj.51.676
PMID:3312702
Abstract

We characterized cardiac myosin isoforms by immunohistochemical approaches using monoclonal antibodies and demonstrated the existence of a distinctive type of cardiac myosin heavy chain which predominates in the fetal stage but is depressed during postnatal development. Furthermore, we showed that this type of cardiac myosin heavy chain was markedly expressed in patients with dilated cardiomyopathy. The results suggested that the pathologic process involved in dilated cardiomyopathy affects myocardial differentiation by the inhibition of the myosin gene switching that normally occurs during muscle maturation. However, we could not find any polymorphism in myosin gene in our population sample of dilated cardiomyopathy. The pathophysiological role of fetal type cardiac myosin expression in dilated cardiomyopathy will be clarified by the characterization of the myosin near future.

摘要

我们使用单克隆抗体通过免疫组织化学方法对心肌肌球蛋白同工型进行了表征,并证明存在一种独特类型的心肌肌球蛋白重链,它在胎儿期占主导地位,但在出生后发育过程中表达降低。此外,我们发现这种类型的心肌肌球蛋白重链在扩张型心肌病患者中显著表达。结果表明,扩张型心肌病所涉及的病理过程通过抑制正常肌肉成熟过程中发生的肌球蛋白基因转换来影响心肌分化。然而,在我们的扩张型心肌病患者群体样本中,未发现肌球蛋白基因存在任何多态性。胎儿型心肌肌球蛋白表达在扩张型心肌病中的病理生理作用将在不久的将来通过对肌球蛋白的表征得以阐明。

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Distribution of cardiac myosin isozymes in cardiomyopathy: immunohistochemical and gene analysis.心肌病中心肌肌球蛋白同工酶的分布:免疫组织化学和基因分析
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引用本文的文献

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Six1 is down-regulated in end-stage human dilated cardiomyopathy independently of Ezh2.Six1在终末期人类扩张型心肌病中下调,且与Ezh2无关。
ESC Heart Fail. 2014 Dec;1(2):154-159. doi: 10.1002/ehf2.12017. Epub 2015 Jan 22.
2
Metabolic gene profile in early human fetal heart development.人类胎儿心脏早期发育中的代谢基因谱
Mol Hum Reprod. 2014 Jul;20(7):690-700. doi: 10.1093/molehr/gau026. Epub 2014 Mar 27.