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| Abnormal Calcium “Sparks” in Cardiomyocytes of Post-myocardial Infarction Heart | |
| 引用本文： | 黄恺,黄丹,付生泉,杨崇哲,廖玉华.Abnormal Calcium “Sparks” in Cardiomyocytes of Post-myocardial Infarction Heart[J].华中科技大学学报(医学英德文版),2008,28(4):401-408. |
| 作者姓名： | 黄恺 黄丹 付生泉 杨崇哲 廖玉华 |
| 作者单位： | Department of Cardiovascular Disease，Institute of Cardiology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology |
| 基金项目： | 国家自然科学基金，国家重点基础研究发展规划(973计划) |
| 摘 要： | In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release （CICR） in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction （MI）. In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium. |
| 关 键 词： | 基因表达 心肌梗死 心血管病 钙渠道 |
Abnormal calcium “Sparks” in cardiomyocytes of post-myocardial infarction heart |
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| Kai Huang,Dan Huang,Shengquan Fu,Chongzhe Yang,Yuhua Liao.Abnormal calcium “Sparks” in cardiomyocytes of post-myocardial infarction heart[J].Journal of Zuazhong University of Science and Technology: Medical Edition,2008,28(4):401-408. | |
| Authors: | Kai Huang Dan Huang Shengquan Fu Chongzhe Yang Yuhua Liao |
| Institution: | 1. Department of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China;Institute of Cardiology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 2. Institute of Cardiology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 3. Department of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China |
| Abstract: | In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium. |
| Keywords: | L calcium channel gene expression myocardial infarction cardiovascular disease |
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