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目的 探讨缝隙连接蛋白在心房纤颤 (房颤 )心房肌的表达及其信号转导机制。方法 6 3例接受开胸手术患者 (包括慢性房颤、阵发性房颤、窦性心律患者 ) ,手术时取心房组织 ,应用逆转录 聚合酶链反应技术检测心房肌钙调磷酸酶调节亚单位 (CalcineurinB)、丝裂原激活的蛋白激酶磷酸酶 1(MKP 1)mRNA表达量 ,采用Western印迹方法 ,检测细胞外调节激酶 1(ERK1)、磷酸化细胞外调节激酶 1(P ERK1)、缝隙连接蛋白 4 0 (Cx4 0 )、缝隙连接蛋白 4 3(Cx4 3)蛋白表达量的改变。结果 慢性房颤、阵发性房颤患者左心房与右心耳组织Cx4 0蛋白表达量 (左心房 :2 2± 0 8,2 2± 0 6 ;右心耳 :2 1± 0 5 ,2 0± 0 8) ,与窦性心律组相比 ,差异有显著意义 (P <0 0 5 )。慢性房颤、阵发性房颤患者Cx4 3蛋白仅在左房组织表达高于窦性心律瓣膜病组 (3 1± 0 6 ,2 8± 0 7vs 1 0± 0 2 ,P均<0 0 5 )。CalcineurinBmRNA、MKP 1mRNA、P ERK1蛋白在慢性房颤、阵发性房颤患者各组的表达水平均明显高于窦性心律组 (P <0 0 5 )。免疫组化显示慢性房颤、阵发性房颤患者Cx4 0、Cx4 3均分布紊乱 ,聚集于细胞的侧边、胞浆或核周。结论 房颤患者心房肌Cx4 0、Cx4 3蛋白基因表达增高且分布异常 ,可能与ERK1及一些磷酸酶的异?
Objective To investigate the expression of connexin in atrial fibrillation (atrial fibrillation) and its signal transduction mechanism. Methods Twenty-three patients undergoing thoracotomy (including chronic atrial fibrillation, paroxysmal atrial fibrillation and sinus rhythm) were enrolled in this study. Atrial tissue was removed during operation. Reverse transcription-polymerase chain reaction (RT-PCR) (Calcineurin B) and mitogen-activated protein kinase phosphatase 1 (MKP 1) mRNA were detected by Western blotting. The expressions of ERK1, P ERK1, The changes of the expression of connexin 4 0 (Cx40) and connexin 4 3 (Cx43) protein were analyzed. Results The expression of Cx40 protein in left atrium and right atrial appendage of patients with chronic atrial fibrillation and paroxysmal atrial fibrillation (left atrium: 2 2 ± 0 8,2 2 ± 0 6; right atrial appendage 2 1 ± 0 5, 2 0 ± 0 8), compared with sinus rhythm group, the difference was significant (P <0 05). The expression of Cx4 3 protein in patients with chronic atrial fibrillation and paroxysmal atrial fibrillation was higher than that in patients with sinus rhythm only in the left atrium (3 1 ± 0 6, 2 8 ± 0 7 vs 1 0 ± 0 2, P <0 0 5). The expression levels of CalcineurinB mRNA, MKP 1 mRNA and P ERK1 protein in patients with chronic atrial fibrillation and paroxysmal atrial fibrillation were significantly higher than those in sinus rhythm group (P <0.05). Immunohistochemistry showed that patients with chronic atrial fibrillation, paroxysmal atrial fibrillation Cx40, Cx4 3 were disrupted, gathered in the side of the cell, cytoplasm or perinuclear. Conclusion Atrial fibrillation patients with atrial fibrillation Cx40, Cx4 3 protein gene expression increased and abnormal distribution, may be associated with ERK1 and some phosphatase?