肺静脉源性房颤模型中L型钙通道α1、α2亚基mRNA表达的研究(PDF)
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2005年第3期
- 页码:
- 213-215
- 栏目:
- 基础研究
- 出版日期:
- 2005-05-05
文章信息/Info
- Title:
- The mRNA expressions of Ltype calcium channel subunit α1 and α2 in the animal model with atrial fibrillation of pulmonary vein source
- Author(s):
- LIU Jun1; ZHU Miaozhang2; ZHENG Qiangsun1; LU Shaoping1; HE Yong1; GUO Haitao2; BI Hui2
- 1.Department of Cardiology, Tangdu Hospital, Fourth Military Medical University，Xi′an, Shaanxi 710038, China
- 分类号:
- R541.7
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的 研究肺静脉源性房颤动物模型中L型钙通道α1、α2亚基mRNA的表达，以阐明肺静脉源性房颤发生的分子机制。 方法 通过建立兔肺静脉源性房颤的动物模型，按房颤持续时间的不同分组，应用半定量逆转录聚合酶链反应测定各实验组的兔肺静脉和心房组织L型钙通道α1、α2亚基mRNA表达水平。 结果 随着房颤持续时间的延长（0.5～6 h），兔肺静脉和心房组织L型钙通道α1亚基mRNA表达水平逐渐下调，至房颤发生后2 h时, 较对照组差异有显著性（P<0.05）；而同样实验条件下，兔肺静脉和心房组织L型钙通道α2亚基mRNA表达水平未出现明显变化，与对照组比较无显著性差异（P>0.05）。 结论 兔肺静脉和心房组织L型钙通道α1亚单位基因转录下调可能是肺静脉源性房颤所致肺静脉和心房电重构的中心机制之一，而在引起L型钙通道功能性下调的因素中，其辅助性亚单位α2所起的调节作用较小。
- Abstract:
- AIM To investigate the mRNA expressions of Ltype calcium channel subunit α1 and α2 in the animal model with atrial fibrillation of pulmonary vein source so as to elucidute the molecular mechanism of that atrial fibrilation. METHODS After the animal models with atrial fibrillation of pulmonary vein source were set up, the rabbits were divided into different groups according to the duration of atrial fibrillation. The gene expressions of Ltype calcium channel subunit α1 and α2 in pulmonary vein and atrial were measured respectively by reverse transcriptionpolymerase chain reation (RTPCR) in six groups. RESULTS The mRNA level of Ltype calcium channel α1 decreased gradually during 0.5 to 6 hours with the lasting of atrial fibrillation. A significant difference was observed 2 hours after the onset of the atrial fibrillation （P<0.05）; and in the same conditions, the mRNA level of Ltype calcium channel α2 remained unchanged in the pulmonary vein and atrial of rabbits（P>0.05）compared with the control group. CONCLUSION The transcription downregulation of Ltype calcium channel α1 gene may be one of mechanisms of electrical remodeling caused by atrial fibrillation of pulmonary vein source, and the accessory subunit α2 may not participate in the functional regulation of Ltype calcium channel.
参考文献/References
［1］Haissaguerre M, Sanders P, Hocini M, et al.Pulmonary veins in the substrate for atrial fibrillation:the "venous wave" hypothesis［J］. J Am Coll Cardiol, 2004,43(12):2290-2292.
［2］Chen YJ, Chen SA, Chen YC, et al. Effects of atrial pacing on arrhythmogenic activity of singlecardiomyocytes from pulmonary veins: implication in initiation of atrial fibrillation［J］. Circulation, 2001,104:2849-2854.
［3］Allessie M, Ausma J, Schotten U. Electrical, contractile and structural remodeling during atrial fibrillation［J］. Cardiovase Res, 2002,54:230-246.
［4］Bosch RF, Zeng XY,Gammer JB, et al. Ionic mechanisms of electrical remodeling in human atrial fibrillation［J］. Cardiovasc Res, 1999,44:121-131.
［5］Ralph F, Bosch RF, Constanze R, et al. Molecular mechanisms of early electrical remodeling: transcriptional downregulation of ion channel subunits reduces Ica,L and Ito in rapid atrial pacingin rabbits［J］. JAAC, 2003,41:858-869.
［6］Van der Velden HMW, Van der Zee L, Wijffels MC, et al. Atrial fibrillation in the goat induces changes in monophasic action potential and mRNA expression of ion channels involved in repolarization ［J］. J Cardiovasc Electrophysiol, 2000, 11:1262-1276.
［7］ Grammer JB, Bosch RF, Kuhlkamp V, et al. Molecular and electrophysiological evidence for “remodeling” of the Ltype Ca2+ channel in persistent atrial fibrillation in humans［J］. Z Kardiol,2000, (Suppl 4) 89:Ⅳ23-Ⅳ29.
备注/Memo
- 备注/Memo:
- 收稿日期：2004-08-28.基金项目：军队“十五”卫生科研基金课题（编号01MB126）
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