miR-5572转基因小鼠构建病态窦房结综合征疾病模型的繁殖与鉴定  

Breeding and genotyping of a miR-5572 transgenic mouse model of sick sinus syndrome

作　　者：张进[1] 李颖[1] 范洁[1] 

机构地区：[1]云南省第一人民医院昆明理工大学附属医院心内科,昆明650000

出　　处：《中国实验动物学报》2017年第5期467-472,共6页Acta Laboratorium Animalis Scientia Sinica

基　　金：国家自然科学基金项目(81360039,81260038);云南省心律失常诊治研究中心基金(No.2014NS260,2014NS259)

摘　　要：目的探讨miR-5572转基因小鼠构建病态窦房结综合征疾病模型的可行性。方法繁殖与鉴定了miR-5572 F1及F2代野生型纯合子及杂合子小鼠,并通过形态学、心电图记录及窦房结组织Cav1.2、Cav1.3mRNA和蛋白表达水平测定来观察疾病模型。结果 F2代miR-5572纯合子敲入小鼠在形态上较野生型小鼠生长缓慢,体型较小。相较于杂合子和野生型小鼠,纯合小鼠的平均心率明显偏低(P<0.05),差异有显著性。miR-5572纯合子小鼠窦房结组织Cav1.2、Cav1.3 mRNA和蛋白表达水平低于野生型(P<0.05),差异有显著性。结论过表达miR-5572转基因小鼠可以构建病态窦房结综合征疾病模型。Objective This study aimed to explore the possibility of establishing a model of sick sinus syndrome by using miR-5572 transgenic mice. Methods F1 and F2 miR-5572 transgenic mice were bred and genotyped,and then observed the phenotype levels of miR-5572 transgenic mice by morphology,electrocardiogram record（ ECG） and the Cav1. 2 and Cav1. 3 expressions levels of mRNA and protein in sinoatrial node tissue of homozygous,heterozygote and wild type mice. Results Compared with the wild type and heterozygous mice,the miR-5572 homozygous mice showed a development delay and smaller body shape,and had slower average heart rate. The mRNA and protein levels of Cav1. 2 and Cav1. 3 in the sinoatrial node tissues were significantly lower. Conclusions The results of this study indicate that miR-5572 homozygous mice may be an efficient approach to establish the model of sick sinus syndrome

关 键 词：病态窦房结综合征 转基因小鼠 繁殖与鉴定 微小RNA-5572 

分 类 号：Q95-33[生物学—动物学]