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| 沉默CrkL对缺氧/复氧诱导的心肌细胞凋亡和生存力的影响及其机制 | |
| 引用本文： | 张志升,杨东艳,张蕾,李刚,扶艳波. 沉默CrkL对缺氧/复氧诱导的心肌细胞凋亡和生存力的影响及其机制[J]. 第二军医大学学报, 2014, 35(11): 1272-1276 |
| 作者姓名： | 张志升 杨东艳 张蕾 李刚 扶艳波 |
| 作者单位： | 重庆医科大学附属第一医院老年病科心血管病组,重庆医科大学附属第一医院老年病科心血管病组,重庆医科大学附属第一医院老年病科心血管病组,重庆医科大学附属第一医院老年病科心血管病组,重庆医科大学附属第一医院老年病科心血管病组 |
| 基金项目： | ] 重庆市卫生局医学科学技术研究项目(2009-2-290, 04-2-154),重庆市科委自然科学基金计划资助项目(CSTC 2007BB5276).Supported by the Medical Science Technology Research Project of Chongqing Health Bureau (2009-2-290 , 04-2-154) and the Natural Science Foundation of Chongqing Science Technology Commission (CSTC2007BB5276). |
| 摘 要： | 目的探讨沉默CrkL对缺氧/复氧诱导的心肌细胞凋亡和生存力的影响及其机制。方法分别用空白试剂、阴性慢病毒和CrkL RNAi慢病毒(沉默CrkL mRNA)感染H9C2心肌细胞,并进行缺氧/复氧(H/R)干预。实验分为空白组、阴性病毒组、CrkL沉默组、空白+H/R组、阴性病毒+H/R组、CrkL沉默+H/R组。用RT-PCR法检测心肌细胞CrkL mRNA的表达,蛋白印迹分析法检测心肌细胞CrkL蛋白、p-ERK1/2蛋白表达,MTT法检测细胞的增殖率,流式细胞术检测细胞的凋亡率。结果 CrkL沉默组较空白组和阴性病毒组,CrkL沉默+H/R组较空白+H/R组和阴性病毒+H/R组CrkL mRNA、CrkL蛋白、p-ERK1/2蛋白、细胞增殖率均降低(P<0.05或P<0.01),细胞凋亡率均增加(P<0.01)。结论沉默CrkL能加重缺氧/复氧诱导的心肌细胞凋亡和生存力降低。该过程可能是由p-ERK1/2蛋白表达降低介导的。 |
| 关 键 词： | CrkL 心肌细胞 细胞凋亡 细胞存活 缺氧/复氧 |
| 收稿时间： | 2014-02-18 |
| 修稿时间： | 2014-07-26 |
Effect of CrkL silence on hypoxia/reoxygenation-induced apoptosis and survival inhibition in cardiomyocytes and the underlying mechanisms |
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| ZHANG Zhi-sheng,YANG Dong-yan,ZHANG Lei,LI Gang and FU Yan-bo. Effect of CrkL silence on hypoxia/reoxygenation-induced apoptosis and survival inhibition in cardiomyocytes and the underlying mechanisms[J]. Former Academic Journal of Second Military Medical University, 2014, 35(11): 1272-1276 | |
| Authors: | ZHANG Zhi-sheng YANG Dong-yan ZHANG Lei LI Gang FU Yan-bo |
| Affiliation: | Division of Cardiology, Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China,,,Division of Cardiology, Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China, |
| Abstract: | Objective To investigate the effect of CrkL silence on hypoxia/reoxygenation (H/R) induced apoptosis and survival inhibition in cardiomyocytes and its underlying mechanisms. Methods H9C2 cardiomyocytes were infected with blank,negative lentivirus and CrkL RNAi lentivirus (CrkL mRNA silence), then treated with H/R respectively. The cardiomyocytes were divided into blank group, negative lentivirus group, CrkL silence group, blank H/R group, negative lentivirus H/R group and CrkL slience H/R group. The expression of CrkL mRNA was detected by RT-PCR, and the expression of CrkL and p-ERK1/2 protein was detected by Western blotting analysis. The apoptosis rate of cardiomyocytes was analyzed by flow cytometry, and the cell proliferation rate was analyzed by MTT. Results Compared with blank negative lentivirus groups and blank H/R negative lentivirus H/R groups, CrkL mRNA protein, p-ERK1 protein, p-ERK1/2 protein and proliferation rate were |
| Keywords: | CrkL H9C2 cardiac myocytes apoptosis cell survival hypoxia/reoxygenation |
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