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压力超负荷对大鼠左室心肌CaMKⅡ和pCREB表达的影响 被引量：1

Role of CaMKⅡ and p-CREB in pressure overload induced hypertrophic rat hearts
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摘要 目的探讨钙调素激酶Ⅱ(CaMKⅡ)和磷酸化核转录因子CREB(pCREB)在压力超负荷大鼠左室心肌中表达的变化。方法100只健康雄性SD大鼠随机分为对照组(n=50)和心肌肥厚组(n=50),制备腹主动脉缩窄大鼠心肌肥厚模型,手术后4周以免疫组化法观察左室心肌CaMKⅡ及pCREB蛋白表达及分布,RT-PCR法检测左室心肌组织bcl2-mRNA含量。结果CaMKⅡ分布于细胞核和细胞浆,pCREB主要分布于细胞核,心肌肥厚组CaMKⅡ和pCREB吸光值显著高于对照组(CaMKⅡ:21.0±0.6vs15.5±0.9;pCREB:16.4±0.7vs11±0.7;P<0.05);心肌肥厚组bcl-2的mRNA表达显著低于对照组(0.52±0.07vs0.68±0.09,P<0.05)。结论压力超负荷时CaMKⅡ激活,核转录因子CREB磷酸化增加,可能通过下调抗凋亡基因bcl-2表达参与心肌肥厚的发生。 AIM To explore the role of calmodolin dependent protein kinaseⅡ and phosphorylation nuclear transcription factor CREB in the development of myocardial hypertrophy. METHODS The model of hypertensive rats was established by abdominal aortic constriction. CaMK Ⅱ and pCREB protein expressions of left ventricular tissue were analyzed by immunohistochemistry method, bcl-2 messenger ribonucleic acid （mRNA） expression of left ventricular tissue was analyzed by reverse transcription PCR （RT-PCR） method. RESULTS CaMK Ⅱ was expressed in both myocardial nuclei myocardial cytoplasmic while pCREB was mainly expressed in myocardial nuclei. The levels of CaMK Ⅱ and pCREB were significantly higher in cardiac hypertrophy group compared with those in control group. The decrease in bcl-2 mRNA expression was found in cardiac hypertrophy group. CONCLUSION CaMK Ⅱ and pCREB may be involved in the development of overload induced cardiac hypertrophy.
作者 周骐 肖颖彬 刘健 王培勇 陈林 钟前进 王学锋
机构地区 第三军医大学新桥医院心外科 第三军医大学病理生理学教研室
出处 《心脏杂志》 CAS 2006年第3期249-252,共4页 Chinese Heart Journal
基金 国家自然科学基金项目资助(No.30200108)
关键词 心肌肥厚 钙调素激酶 凋亡 核转录因子 cardiac hypertrophy calmodulin dependent protein kinase apoptosis nuclear transcription factory
分类号 R542.2 [医药卫生—心血管疾病]
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参考文献13

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共引文献8

同被引文献21

  • 1周骐,肖颖彬,王培勇,陈林,钟前进,王学锋,刘健.心肌肥厚大鼠左室心肌CaMKⅣ改变的意义[J].重庆医学,2005,34(9):1347-1349. 被引量：4
  • 2周骐,肖颖彬,刘健,王培勇,陈林,钟前进,王学锋.心肌细胞核钙调素I介导的bcl-2转录调节在大鼠心肌肥厚中的作用[J].生理学报,2005,57(6):731-736. 被引量：3
  • 3周骐,肖颖彬,刘健,王培勇,陈林,钟前进,王学锋.心肌细胞核钙调素Ⅰ和CREB磷酸化在压力负荷大鼠心肌肥厚中的作用[J].高血压杂志,2006,14(1):52-56. 被引量：4
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心脏杂志
2006年 第3期

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