[1]周胜凯,秦川,陈林,等.EPO对慢性缺氧心肌细胞线粒体生物合成的影响[J].第三军医大学学报,2013,35(12):1192-1196.
 Zhou Shengkai,Qin Chuan,Chen Lin,et al.Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro[J].J Third Mil Med Univ,2013,35(12):1192-1196.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
35卷
期数:
2013年第12期
页码:
1192-1196
栏目:
论著
出版日期:
2013-06-30

文章信息/Info

Title:
Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro
作者:
周胜凯秦川陈林肖颖彬
第三军医大学新桥医院全军心血管外科研究所
Author(s):
Zhou Shengkai Qin Chuan Chen Lin Xiao Yingbin
Institute of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China
关键词:
促红细胞生成素慢性缺氧线粒体生物合成蛋白激酶B(Akt)内皮型一氧化氮合酶(eNOS)
Keywords:
erythropoietin chronic hypoxia mitochondrial biogenesis Akt endothelial nitric oxide synthase
分类号:
R322.11;R329.26;R364.4
文献标志码:
A
摘要:
目的      观察促红细胞生成素(erythropoietin, EPO)在慢性缺氧条件下对心肌线粒体生物合成的影响及其可能的机制。      方法      将H9c2心肌细胞株置入缺氧培养箱7 d(94% N2,5%CO2,1%O2),建立H9c2心肌细胞株慢性缺氧模型;采用5、10、20 U/mL不同浓度的rhEPO(recombinant human erythropoietin;重组人促红细胞生成素)干预处理后,用荧光探针标记线粒体,观察线粒体数目的变化;RT-PCR技术检测线粒体DNA的相对拷贝数变化;Western blot技术检测Akt、eNOS及其磷酸化蛋白水平的变化。      结果      rhEPO干预7 d后线粒体数目及拷贝数增加(P<0.05);Akt、eNOS蛋白磷酸化水平增强(P<0.05),Akt、eNOS总蛋白无明显变化(P>0.05)。      结论      EPO增强了慢性缺氧心肌细胞的线粒体生物合成,Akt、eNOS可能是EPO增强线粒体生物合成的重要信号通路。
Abstract:
Objective      To determine the effect of erythropoietin (EPO) on the mitochondrial biogenesis in rat cardiomyocytes under the condition of chronic hypoxia.       Methods      Rat cardiomyocyte-derived H9c2 cells were deprived of oxygen for 7 d to establish the chronic hypoxia model (94% N2, 5%CO2 and 1%O2). Then the obtained H9c2 cells were treated by recombinant human EPO (rhEPO, 5, 10 and 20 U/ml) for 3 or 7 d. Fluorescent probe was used to mark mitochondria in the cells for the amount of mitochondria. The protein levels of Akt, phospho-Akt (serine473), endothelial nitric oxide synthase (eNOS), and phospho-eNOS (serine1177) were determined with Western blotting. RT-PCR was used to detect the relative copy number of mitochondrial DNA.       Results      rhEPO treatment for 7 d resulted in a significant increase in the amount and copy number of mitochondria (P<0.05). The phosphorylation levels of Akt and eNOS were also enhanced, but those of akt and eNOS had no change (P>0.05).       Conclusion      EPO improves mitochondrial biogenesis in the cardiomyocytes exposure to chronic hypoxia, probably through Akt and eNOS signal transduction.

参考文献/References:

周胜凯, 秦川, 陈林, 等. EPO对慢性缺氧心肌细胞线粒体生物合成的影响[J].第三军医大学学报,2013,35(12):1192-1196.

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更新日期/Last Update: 2013-06-20