Cx40和PGP9.5在人肺静脉肌袖中的表达及其意义
发布时间：2018-08-11 13:58
【摘要】： 研究背景与目的:心房纤颤(房颤,atrial fibrillation)的发病机制是多因素的,目前尚未完全阐明。新近的大量研究表明,肺静脉肌袖和房颤之间存在着密切关系。肺静脉肌袖(myocardial sleeves of pulmonary veins)是指缠绕于与心房相连的肺静脉主干根部的心肌组织,是作为异位兴奋灶引发局灶性房颤的关键解剖部位。胚胎期的肺静脉存在自律性,而且,肺静脉肌袖组织在发育过程中有与心脏传导系统相同的抗原表达。神经元特异性抗原PGP9.5(protein gene product 9.5)是一种古老而保守的蛋白质,已发现多种动物的窦房结、房室结、希氏束、左右束支和浦肯野纤维中PGP9.5表达阳性率显著高于临近的心肌细胞。研究还发现,房颤可导致心肌电生理改变,影响蛋白表达及引起组织学变化,特别是缝隙连接蛋白表达量的变化及其在细胞间的重新分布,即缝隙连接重构,与房颤的稳定性增加有关。本研究探讨正常人肺静脉肌袖以及风湿性心脏病房颤患者肺静脉肌袖中缝隙连接蛋白40 (Cx40)和PGP9.5抗原表达和分布的特征及其临床病理意义。 方法:15例风湿性心脏病房颤患者,瓣膜置换术时取左上肺静脉肌袖组织;20例窦性心律无心脏疾病死亡的尸检者,取其左上肺静脉肌袖组织。行HE染色及二步法免疫组织化学染色观察PGP9.5抗原表达和组织学特点;用奥林巴斯BX41免疫荧光显微镜观察连接蛋白40(Cx40)表达和分布的改变。 结果: 1. HE染色显示,肺静脉肌袖存在明显的纤维化。窦律组肺静脉肌袖中存在水肿和空泡样变性的心肌细胞,在6例肺静脉肌袖组织中观察到染色浅淡的P样细胞,单个或成群出现;房颤组肺静脉肌袖组织中未发现P样细胞。 2.免疫组织化学染色显示,窦律组10例、房颤组1例肺静脉肌袖组织中存在PGP9.5免疫组织化学染色阳性的特化心肌细胞和神经纤维。 3.奥林巴斯BX41免疫荧光显微镜观察到Cx40在12例窦律组肺静脉肌袖组织中呈现均匀分布,在细胞之间端端连接的闰盘处分布较多。水肿、空泡样变性的心肌细胞和特化心肌细胞的Cx40蛋白分布发生变化,端端即闰盘处分布减少,而侧侧分布增加。Cx40在10例房颤组肺静脉肌袖组织中的分布模式发生了显著改变,端端分布减少,而侧侧分布明显增加。 结论: 1.肺静脉肌袖组织的一些特殊细胞与心脏传导系统有相同的PGP9.5抗原表达。 2.肺静脉肌袖组织Cx40再分布可能与风湿性心脏病房颤的发生和维持有关。 3.肺静脉肌袖组织Cx40蛋白质再分布可能与心肌细胞和特化心肌细胞的水肿、变性有关。
[Abstract]:Background & objective: the pathogenesis of atrial fibrillation (fibrillation) is multivariate and has not been fully elucidated. A large number of recent studies have shown that there is a close relationship between pulmonary venous cuff and atrial fibrillation. Pulmonary vein muscle sleeve (myocardial sleeves of pulmonary veins) is a kind of myocardial tissue which is entwined in the root of pulmonary vein trunk which is connected to the atrium. It is the key anatomic site of focal atrial fibrillation caused by ectopic excitatory foci. The pulmonary vein at embryonic stage has the same antigen-expression as the cardiac conduction system in the development of pulmonary vein muscle cuff tissue. Neuron specific antigen (PGP9.5 (protein gene product 9.5) is an ancient and conserved protein. It has been found that the positive rate of PGP9.5 expression in sinoatrial node, atrioventricular node, Hickland bundle, left and right bundle branches and Purkinje fibers in many animals is significantly higher than that in adjacent cardiomyocytes. It was also found that atrial fibrillation can cause electrophysiological changes in myocardium, affect protein expression and cause histological changes, especially the change of gap junction protein expression and its redistribution between cells, that is, gap junction remodeling. Associated with increased stability of atrial fibrillation. The aim of this study was to investigate the expression and distribution of gap junction protein 40 (Cx40) and PGP9.5 antigens in pulmonary venous muscle cuff and atrial fibrillation patients with rheumatic heart disease and its clinicopathological significance. Methods in 15 patients with rheumatic atrial fibrillation, 20 patients with left superior pulmonary vein muscle cuff tissue and 20 patients died of sinus arrhythmia without heart disease were examined during valvular replacement, and the left superior pulmonary vein muscle cuff tissue was taken. The expression and histological characteristics of PGP9.5 antigen were observed by HE staining and two step immunohistochemical staining, and the changes of Cx40 expression and distribution were observed by Olympus BX41 immunofluorescence microscope. Results: 1. He staining showed that pulmonary vein muscle cuff had obvious fibrosis. In the sinus rhythm group, there were edema and vacuolar degeneration in pulmonary venous muscle cuff. P-like cells were not found in pulmonary vein cuff tissue of atrial fibrillation group. 2. 2. Immunohistochemical staining showed that 10 cases in sinus rhythm group and 1 case in atrial fibrillation group had specific myocardial cells and nerve fibers positive for PGP9.5 immunohistochemical staining. Olympus BX41 immunofluorescence microscopy showed that Cx40 was uniformly distributed in pulmonary venous muscle cuff tissue in 12 cases of sinus rhythm group, and was more distributed in intercalated disc with end to end connection between cells. The distribution of Cx40 protein in cardiomyocytes with edema, vacuolar degeneration and specialized cardiomyocytes was changed. The distribution of Cx40 protein at the end and intercalated disc decreased, while the distribution pattern of Cx40 in 10 patients with atrial fibrillation was significantly changed, and the distribution of Cx40 was increased in 10 patients with atrial fibrillation. The end-end distribution decreased, while the side-side distribution increased significantly. Conclusion: 1. Some special cells of pulmonary vein muscle cuff tissue have the same PGP9.5 antigen expression as heart conduction system. 2. The redistribution of Cx40 in pulmonary vein muscle cuff tissue may be related to the occurrence and maintenance of atrial fibrillation in rheumatic heart disease. 3. The redistribution of Cx40 protein in pulmonary vein muscle cuff may be related to edema and degeneration of cardiomyocytes and specialized cardiomyocytes.
【学位授予单位】：大连医科大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R363
本文编号：2177189
[Abstract]:Background & objective: the pathogenesis of atrial fibrillation (fibrillation) is multivariate and has not been fully elucidated. A large number of recent studies have shown that there is a close relationship between pulmonary venous cuff and atrial fibrillation. Pulmonary vein muscle sleeve (myocardial sleeves of pulmonary veins) is a kind of myocardial tissue which is entwined in the root of pulmonary vein trunk which is connected to the atrium. It is the key anatomic site of focal atrial fibrillation caused by ectopic excitatory foci. The pulmonary vein at embryonic stage has the same antigen-expression as the cardiac conduction system in the development of pulmonary vein muscle cuff tissue. Neuron specific antigen (PGP9.5 (protein gene product 9.5) is an ancient and conserved protein. It has been found that the positive rate of PGP9.5 expression in sinoatrial node, atrioventricular node, Hickland bundle, left and right bundle branches and Purkinje fibers in many animals is significantly higher than that in adjacent cardiomyocytes. It was also found that atrial fibrillation can cause electrophysiological changes in myocardium, affect protein expression and cause histological changes, especially the change of gap junction protein expression and its redistribution between cells, that is, gap junction remodeling. Associated with increased stability of atrial fibrillation. The aim of this study was to investigate the expression and distribution of gap junction protein 40 (Cx40) and PGP9.5 antigens in pulmonary venous muscle cuff and atrial fibrillation patients with rheumatic heart disease and its clinicopathological significance. Methods in 15 patients with rheumatic atrial fibrillation, 20 patients with left superior pulmonary vein muscle cuff tissue and 20 patients died of sinus arrhythmia without heart disease were examined during valvular replacement, and the left superior pulmonary vein muscle cuff tissue was taken. The expression and histological characteristics of PGP9.5 antigen were observed by HE staining and two step immunohistochemical staining, and the changes of Cx40 expression and distribution were observed by Olympus BX41 immunofluorescence microscope. Results: 1. He staining showed that pulmonary vein muscle cuff had obvious fibrosis. In the sinus rhythm group, there were edema and vacuolar degeneration in pulmonary venous muscle cuff. P-like cells were not found in pulmonary vein cuff tissue of atrial fibrillation group. 2. 2. Immunohistochemical staining showed that 10 cases in sinus rhythm group and 1 case in atrial fibrillation group had specific myocardial cells and nerve fibers positive for PGP9.5 immunohistochemical staining. Olympus BX41 immunofluorescence microscopy showed that Cx40 was uniformly distributed in pulmonary venous muscle cuff tissue in 12 cases of sinus rhythm group, and was more distributed in intercalated disc with end to end connection between cells. The distribution of Cx40 protein in cardiomyocytes with edema, vacuolar degeneration and specialized cardiomyocytes was changed. The distribution of Cx40 protein at the end and intercalated disc decreased, while the distribution pattern of Cx40 in 10 patients with atrial fibrillation was significantly changed, and the distribution of Cx40 was increased in 10 patients with atrial fibrillation. The end-end distribution decreased, while the side-side distribution increased significantly. Conclusion: 1. Some special cells of pulmonary vein muscle cuff tissue have the same PGP9.5 antigen expression as heart conduction system. 2. The redistribution of Cx40 in pulmonary vein muscle cuff tissue may be related to the occurrence and maintenance of atrial fibrillation in rheumatic heart disease. 3. The redistribution of Cx40 protein in pulmonary vein muscle cuff may be related to edema and degeneration of cardiomyocytes and specialized cardiomyocytes.
【学位授予单位】：大连医科大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R363
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