我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

压力超负荷对大鼠左室心肌CaMKⅡ和pCREB表达的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第3期
页码:
249-252
栏目:
基础研究
出版日期:
2006-06-25

文章信息/Info

Title:
Role of CaMKⅡ and pCREB in pressure overload induced hypertrophic rat hearts
作者:
周骐1; 肖颖彬1; 刘健1; 王培勇2; 陈林1; 钟前进1; 王学锋1
第三军医大学：1.新桥医院心外科，重庆 400037，2.病理生理学教研室，重庆 400038
Author(s):
ZHOU Qi1;  XIAO Ying-bin1;  LIU Jian1;  WANG Pei-yong2;  CHEN Lin1;  ZHONG Qian-jin1;  WANG Xue-feng1
1.Department of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China, 2.Department of Pathophysiology, Third Military Medical University, Chongqing, 400038, China
关键词:
心肌肥厚; 钙调素激酶; 凋亡; 核转录因子
Keywords:
cardiac hypertrophy;  calmodulin dependent protein kinase;  apoptosis;  nuclear transcription factory
分类号:
R542.2
DOI:
-
文献标识码:
A
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bcl-2 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±0.6 vs 15.5±0.9；pCREB：16.4±0.7 vs 11±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±0.07 vs 0.68±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。
Abstract:
AIM To explore the role of calmodolin dependent protein kinase Ⅱ and phosphorylation nuclear transcription factor CREB in the development of myocardial hypertrophy. METHODS The model of hypertensive rats was established by abdominal aortic constriction. CaMKⅡ 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 CaMKⅡ was expressed in both myocardial nuclei myocardial cytoplasmic while pCREB was mainly expressed in myocardial nuclei. The levels of CaMKⅡ 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 CaMKⅡ and pCREB may be involved in the development of overload induced cardiac hypertrophy.

参考文献/References

［1］ 张春虹，臧伟进，臧益民. RAS系统、Ca2+转运与糖尿病心肌病的关系［J］. 心脏杂志，2002, 14（5): 439-442.

［2］ Zolk O, Marx M, Jackel E, et al. Betaadrenergic stimulation induces cardiac ankyrin repeat protein expression: involvement of protein kinase A and calmodulindependent kinase［J］. Cardiovasc Res, 2003, 59（3): 563-572.

［3］ Gusterson RJ, Jazrawi E, Adcock IM, et al. The transcriptional coactivators CREBbinding protein (CBP) and p300 play a critical role in cardiac hypertrophy that is dependent on their histone acetyltransferase activity ［J］. J Biol Chem, 2003, 278（9): 6838-6847.

［4］ Mehrhof FB, Muller FU, Bergmann MW, et al. In cardiomyocyte hypoxia, insulinlike growth factorIinduced antiapoptotic signaling requires hosphatidylinositol3OHkinasedependent and mitogenactivated protein kinasedependent activation of the transcription factor cAMP response elementbinding protein ［J］. Circulation, 2001, 104（17): 2088-2094.

［5］ Ohkusa T, Hisamatsu Y, Yano M, et al. Altered cardiac mechanism and sarcoplasmic reticulum function in pressure overloadinduced cardiac hypertrophy in rats ［J］. J Mol Cell Cardiol, 1997, 29（1): 45-54.

［6］ Forte A, Esposito s, De Feo M, et al. Stenosis progression after surgical injury in Milan hypertensive rat carotid arteries ［J］. Cardiovascular Research, 2003, 60（3): 654-663.

［7］ Nakanishi K, Nakata Y, Kanazawa F, et al. Changes in myosin heavy chain and its localization in rat heart in association with hypobaric hypoxiainduced pulmonary hypertension ［J］. J Pathol, 2002, 197（3): 380-387.

［8］ Maier LS, Bers DM. Calcium, calmodulin, and calcium calmodulin kinase II: heartbeat to heartbeat and beyond ［J］. J Mol Cell Cardiol, 2002, 34(8): 919-939.

［9］ Colomer JM, Mao L, Rockman HA, et al. Pressure overload selectively upregulates Ca2+/calmodulindependent protein kinase II in vivo ［J］. Mol Endocrinol, 2003, 17（2): 183-192.

［10］Wu Y, Temple J, Zhang R, et al. Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophy ［J］. Circulation, 2002, 106（10): 1288-1293.

［11］El JA, Freund C, Rechner C, et al. Reoxygenation after severe hypoxia induces cardiomyocyte hypertrophy in vitro: activation of CREB downstream of GSK3beta ［J］. FASEB J, 2004, 18（10): 1096-1098.

［12］Fladmark KE, Brustugun OT, Mellgren G, et al. Ca2+/calmodulindependent protein kinase II is required for microcystininduced apoptosis ［J］. J Biol Chem, 2002, 277（4): 2804-2811.

［13］ Imamura ST，Matsuoka R,Hiratsuka E,et al. Adaptational changes of MHC gene expression and isozyme transition in cardiac overloading［J］. Am J Physiol, 1991,260(1 pt 2):H73-H79.

备注/Memo

备注/Memo:
收稿日期：2005-05-31.基金项目：国家自然科学基金项目资助（No.30200108）通讯作者：肖颖彬，主任医师，教授，主要从事体循环病理研究 Tel:(023)68755607 Email:xioyb@vip.sina.com 作者简介：周骐，博士生，主治医师 Tel：（023）68774607 Email：Drzhouqi@21cn.com
更新日期/Last Update: