Cx40和PGP9.5在人肺靜脈肌袖中的表達及其意義
發(fā)布時間：2018-08-11 13:58
【摘要】： 研究背景與目的:心房纖顫(房顫,atrial fibrillation)的發(fā)病機制是多因素的,目前尚未完全闡明。新近的大量研究表明,肺靜脈肌袖和房顫之間存在著密切關系。肺靜脈肌袖(myocardial sleeves of pulmonary veins)是指纏繞于與心房相連的肺靜脈主干根部的心肌組織,是作為異位興奮灶引發(fā)局灶性房顫的關鍵解剖部位。胚胎期的肺靜脈存在自律性,而且,肺靜脈肌袖組織在發(fā)育過程中有與心臟傳導系統(tǒng)相同的抗原表達。神經(jīng)元特異性抗原PGP9.5(protein gene product 9.5)是一種古老而保守的蛋白質(zhì),已發(fā)現(xiàn)多種動物的竇房結(jié)、房室結(jié)、希氏束、左右束支和浦肯野纖維中PGP9.5表達陽性率顯著高于臨近的心肌細胞。研究還發(fā)現(xiàn),房顫可導致心肌電生理改變,影響蛋白表達及引起組織學變化,特別是縫隙連接蛋白表達量的變化及其在細胞間的重新分布,即縫隙連接重構,與房顫的穩(wěn)定性增加有關。本研究探討正常人肺靜脈肌袖以及風濕性心臟病房顫患者肺靜脈肌袖中縫隙連接蛋白40 (Cx40)和PGP9.5抗原表達和分布的特征及其臨床病理意義。 方法:15例風濕性心臟病房顫患者,瓣膜置換術時取左上肺靜脈肌袖組織;20例竇性心律無心臟疾病死亡的尸檢者,取其左上肺靜脈肌袖組織。行HE染色及二步法免疫組織化學染色觀察PGP9.5抗原表達和組織學特點;用奧林巴斯BX41免疫熒光顯微鏡觀察連接蛋白40(Cx40)表達和分布的改變。 結(jié)果: 1. HE染色顯示,肺靜脈肌袖存在明顯的纖維化。竇律組肺靜脈肌袖中存在水腫和空泡樣變性的心肌細胞,在6例肺靜脈肌袖組織中觀察到染色淺淡的P樣細胞,單個或成群出現(xiàn);房顫組肺靜脈肌袖組織中未發(fā)現(xiàn)P樣細胞。 2.免疫組織化學染色顯示,竇律組10例、房顫組1例肺靜脈肌袖組織中存在PGP9.5免疫組織化學染色陽性的特化心肌細胞和神經(jīng)纖維。 3.奧林巴斯BX41免疫熒光顯微鏡觀察到Cx40在12例竇律組肺靜脈肌袖組織中呈現(xiàn)均勻分布,在細胞之間端端連接的閏盤處分布較多。水腫、空泡樣變性的心肌細胞和特化心肌細胞的Cx40蛋白分布發(fā)生變化,端端即閏盤處分布減少,而側(cè)側(cè)分布增加。Cx40在10例房顫組肺靜脈肌袖組織中的分布模式發(fā)生了顯著改變,端端分布減少,而側(cè)側(cè)分布明顯增加。 結(jié)論: 1.肺靜脈肌袖組織的一些特殊細胞與心臟傳導系統(tǒng)有相同的PGP9.5抗原表達。 2.肺靜脈肌袖組織Cx40再分布可能與風濕性心臟病房顫的發(fā)生和維持有關。 3.肺靜脈肌袖組織Cx40蛋白質(zhì)再分布可能與心肌細胞和特化心肌細胞的水腫、變性有關。
[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.
【學位授予單位】：大連醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2007
【分類號】：R363
本文編號：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.
【學位授予單位】：大連醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2007
【分類號】：R363
【參考文獻】
相關期刊論文 前7條
1 馬驍;張薇;鐘明;亓同剛;苗雅;孫慧;張運;;心房顫動致犬肺靜脈肌袖縫隙連接蛋白40表達降低[J];基礎醫(yī)學與臨床;2006年04期
2 紀榮明,姜宗來,張炎,秦永文,王志軍,張煜輝,黃章翔,曹鵬;經(jīng)皮穿刺介入肺靜脈射頻消融治療陣發(fā)性房顫的應用解剖[J];解剖學報;2002年06期
3 郭志坤,蔡新華,文小軍,張紅旗;心房顫動的細胞形態(tài)學基礎——右心房的組織學觀察[J];中國心臟起搏與心電生理雜志;1998年01期
4 周自強,胡大一,陳捷,張仁漢,李奎寶,趙秀麗;中國心房顫動現(xiàn)狀的流行病學研究[J];中華內(nèi)科雜志;2004年07期
5 楊延宗,劉瑩,孫雷,李連宏,鄭仁恕,高連君,林治湖;人體肺靜脈組織學觀察12例[J];中華心血管病雜志;2004年05期
6 嚴卉,陳君柱,朱建華,倪一鳴,余國偉,胡申江,陶謙民;縫隙連接蛋白在心房纖顫患者心房肌的表達及其信號轉(zhuǎn)導途徑[J];中華醫(yī)學雜志;2004年03期
7 李大強,馮義柏,張會琴;心房肌間隙連接重構與風濕性瓣膜病患者心房顫動的關系[J];中華醫(yī)學雜志;2004年05期
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