Popdc2在心脏肥大中的表达及其对病理性心脏肥大的影响

魏飞宇; 吕丽; 张进; 王礼琳; 丁立群; 李颖; 范洁

doi:10.13201/j.issn.1001-1439.2018.03.022

Popdc2在心脏肥大中的表达及其对病理性心脏肥大的影响

- 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, 650032);
- 2. 昆明医科大学第二附属医院肿瘤科
基金项目:
国家自然科学基金（No：81260038，81360039）

详细信息

通讯作者: 范洁,E-mail:fanj905@163.com

中图分类号: R542.2

收稿日期: 2017-08-23

The expression of Popdc2 in cardiac hypertrophy and its effects on pathological hypertrophy

- 1. Department of Cardiology, the First People's Hospital of Yunnan Province, the affiliated Hospital of Kunming University of Science and Technology, Kunming, 650032, China;
- 2. Department of Medical Oncology, the Second Affiliated Hospital of Kunming Medical University

More Information

Corresponding author: FAN Jie, E-mail: fanj905@163.com

Received Date: 23 August 2017

摘要

摘要: 目的：探讨心脏胚胎基因——Popdc2在小鼠心脏肥大中的差异表达，研究Popdc2对病理性心脏肥大的保护作用。方法：通过游泳锻炼构建小鼠生理性心脏肥大模型，主动脉缩窄术建立病理性心脏肥大模型，采用异丙肾上腺素（PE）诱导心肌细胞病理性肥大，qRT-PCR和Western blot检测Popdc2及相关基因mRNA和蛋白表达水平，TUNEL实验检测各组心肌细胞凋亡比例。结果：成功构建生理性及病理性心脏肥大模型。和对照组相比，生理性心脏肥大中Popdc2 mRNA （3.64±0.29︰1.08±0.44，P<0.01）和蛋白（0.52±0.04︰0.29±0.03，P<0.01）表达升高，而在病理性心脏肥大中Popdc2 mRNA （0.60±0.05︰1.05±0.13，P<0.05）和蛋白（0.03±0.01︰0.07±0.01，P<0.01）表达下降。心肌细胞病理性肥大的过程中Popdc2 mRNA （0.47±0.05︰1.04±0.08，P<0.01）和蛋白（0.53±0.11︰1.22±0.11，P<0.01）表达也下降。过表达Popdc2可减少病理性心脏肥大过程中的细胞凋亡（0.95±0.07︰1.63±0.11，P<0.01）、病理性标志基因心房利钠肽、B型利钠肽和纤维化蛋白CollagenⅠ、CollagenⅡ的mRNA表达。结论：Popdc2在生理性和病理性心脏肥大中呈现出不一致的变化趋势，且Popdc2可改善心肌细胞的病理性肥大，可能成为区别2种不同心脏肥大分子标志物及成为拮抗病理性心脏肥大、心力衰竭的作用靶点。
- 心脏肥大 /
- 主动脉缩窄术 /
- Popdc2 /
- 凋亡
Abstract: Objective: To explore the expression of Popdc2 in cardiac hypertrophy in mice, and to study the effect of Popdc2 on pathological cardiomyocytes hypertrophy.Method: Physiological cardiac hypertrophy models wre established by swimming training and pathological cardiac hypertrophy models were established by transverse aortic coarctation. Pathological cardiac hypertrophy was induced by isoproterenol (PE) in vitro. Cells apoptosis were detected with TUNEL experiments.The mRNA and protein of ANP, BNP, Popdc2 collagen Ⅰ and Ⅱ (Collagen Ⅰ and Collagen Ⅱ) expression was determined by qRT-PCR and western blot.Result: Physiological and pathological cardiac hypertrophy models were successfully constructed. The expression of Popdc2 mRNA (3.64±0.29 vs 1.08±0.44, P<0.01) and protein (0.52±0.04 vs 0.29±0.03, P<0.01) was increased in physiological cardiac hypertrophy, and the expression of Popdc2 mRNA (0.60±0.05 vs 1.05±0.13, P<0.05) and protein (0.03±0.01 vs 0.07±0.01, P<0.01) was decreased in pathological cardiac hypertrophy in vivo. The expression of Popdc2 mRNA (0.47±0.05 vs 1.04±0.08, P<0.01) and protein (0.53±0.11 vs 1.22±0.11, P<0.01) was decreased in pathological cardiomyocytes hypertrophy in vitro. The cell apoptosis rate (0.95±0.07 vs 1.63±0.11, P<0.01) was reduced and the expression of ANP, BNP, Collagen Ⅰ and Ⅱ mRNA was decreased in over-expression of Ad-Popdc2 group than that in control group.Conclusion: The expression of Popdc2 is not consistent in physiological and pathological cardiac hypertrophy, and overexprssion of Popdc2 ameliorate the pathological cardiac hypertrophy. Popdc2 maybe as a molecular marker between two different cardiac hypertrophy model and become the target of antagonistic pathological cardiac hypertrophy and heart failure.
- cardiac hypertrophy /
- transverse aortic coarctation /
- Popdc2 /
- apoptosis

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