Effect of SERCA2a overexpression in the pericardium mediated by the AAV1 gene transfer on rapid atrial pacing in rabbits
Effect of SERCA2a overexpression in the pericardium mediated by the AAV1 gene transfer on rapid atrial pacing in rabbits
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DOI：
10.4238/2015.october.28.24
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发表时间：
2015-01-01
影响因子：
0.4
通讯作者：
Wulasihan, M. H. Y. T.
中科院分区：
文献类型：
--
作者：
Kuken, B. N.;Aikemu, A. N. W. E.;Wulasihan, M. H. Y. T.
研究肌浆网ATP酶2a（SERCA 2a）基因过表达对新西兰白色兔快速心房起搏（RAP）后SERCA 2a活性及蛋白表达的影响。新西兰白色兔随机分为假手术组（A组）、腺相关病毒1型（AAV 1）/EGFP +房颤（AF）模型组（B组）和AVV 1/SERCA 2a + AF组（C组）。假手术组作为阴性对照。每组由10只动物组成。B和C组分别注射500 μ L的AAV 1-EGFP报告基因和500 μ L的AAV 1-SERCA 2a靶基因。AAV 1介导的基因转移后4周，兔右心房接受24 h RAP。处死动物，采用蛋白质印迹法测定心肌中蛋白质活性和蛋白质表达。4周后，C组SERCA 2a蛋白活性和表达水平显著高于A、B组（P < 0.05）。右心房RAP诱发家兔心房颤动，导致SERCA 2a活性和蛋白表达降低。心包AAV-1介导的SERCA 2a基因转移导致SERCA 2a过表达，恢复SERCA 2a活性和蛋白表达。
To study the effects of overexpression of the sarcoplasmic reticulumATPase 2a (SERCA2a) gene on the activity and protein expression of SERCA2a after rapid atrial pacing (RAP) in New Zealand white rabbits. New Zealand white rabbits were randomly divided into a sham-operated group (group A), adeno-associated virus 1 (AAV1)/EGFP + atrial fibrillation (AF) model group (group B), or AVV1/SERCA2a + AF group (group C). The sham-operated group was used as a negative control. Each group consisted of 10 animals. Groups B and C were injected with 500 pL of the AAV1-EGFP reporter gene and 500 pL of the AAV1-SERCA2a target gene, respectively. Four weeks after AAV1-mediated gene transfer, the rabbits underwent 24 h of RAP to the right atrium. The animals were sacrificed and protein activity and protein expression in the myocardium were measured using the westernblot method. Four weeks after AAV1-mediated gene transfer, SERCA2a protein activity and expression were significantly higher in Group C than in Groups A and B (P < 0.05). RAP of the right atrium induced atrial fibrillation in rabbits, resulting in decreases in the activity and protein expression of SERCA2a. Pericardial AAV-1 mediated SERCA2a gene transfer resulted in the overexpression of SERCA2a, restoring SERCA2a activity and protein expression.