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山羊心房中房颤诱导的细胞结构重塑的时间进程。

Time course of atrial fibrillation-induced cellular structural remodeling in atria of the goat.

作者信息

Ausma J, Litjens N, Lenders M H, Duimel H, Mast F, Wouters L, Ramaekers F, Allessie M, Borgers M

机构信息

Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.

出版信息

J Mol Cell Cardiol. 2001 Dec;33(12):2083-94. doi: 10.1006/jmcc.2001.1472.

DOI:10.1006/jmcc.2001.1472
PMID:11735256
Abstract

BACKGROUND

Previously we documented cellular structural changes of a non-degenerative nature in atrial myocytes after atrial fibrillation (AF) in the goat. The time course of these changes was not studied.

METHODS AND RESULTS

Cellular structural changes were studied by light- and electron microscopy and immunohistochemistry in goat atria after 0-16 weeks AF. The first sign of cellular structural remodeling was a more homogeneous chromatin distribution, at 1 week of AF. Sub-structural changes in mitochondria and sarcoplasmic reticulum occurred gradually. Cellular degeneration was absent. The degree of myolysis and glycogen accumulation increased till 8 weeks of AF and did not increase further from thereon. After 16 weeks of AF, 42% of the myocytes in the right atrial free wall were affected by myolysis. The diameter of the atrial myocytes increased. Dedifferentiation of the atrial myocytes was suggested by altered expression patterns of structural proteins, such as the disappearance of cardiotin (1 week), the A-I junctional part of titin (4 weeks), desmin at the intercalated disk (ID) (8 weeks) and a gradual re-expression of alpha-smooth muscle actin.

CONCLUSION

Remodeling of the cellular ultrastructure in atrial myocardium of the goat develops progressively during AF. Re-expression of fetal proteins indicate dedifferentiation of atrial myocytes, analogous to observations in hibernating myocardium of the ventricle.

摘要

背景

此前我们记录了山羊房颤(AF)后心房肌细胞非退行性的细胞结构变化。但未对这些变化的时间进程进行研究。

方法与结果

通过光学显微镜、电子显微镜和免疫组织化学对山羊房颤0 - 16周后的心房细胞结构变化进行研究。细胞结构重塑的首个迹象是在房颤1周时染色质分布更均匀。线粒体和肌浆网的亚结构变化逐渐发生。未出现细胞变性。肌溶解和糖原积累程度在房颤8周时增加,此后不再进一步增加。房颤16周后,右心房游离壁42%的肌细胞受肌溶解影响。心房肌细胞直径增加。结构蛋白表达模式改变提示心房肌细胞去分化,如心肌膜蛋白(1周)消失、肌联蛋白A - I连接部分(4周)、闰盘处结蛋白(8周)消失以及α - 平滑肌肌动蛋白逐渐重新表达。

结论

山羊心房心肌细胞超微结构重塑在房颤期间逐渐发展。胎儿蛋白的重新表达表明心房肌细胞去分化,类似于心室冬眠心肌中的观察结果。

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