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丝裂素活化蛋白激酶参与钙激动剂介导的心肌肥大(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2002年第4期
页码:
287-289
栏目:
实验研究
出版日期:
2002-07-01

文章信息/Info

Title:
Mitogen activated protein kinase in calcium activator mediated cardiomyocyte hypertrophy
作者:
杨永健1 祝善俊1 祝之明2 胡厚祥2 丁 钢2
第三军医大学西南医院: 1. 新桥医院心内科, 2. 大坪医院高血压中心, 重庆 400038
Author(s):
YANG Yong-jian1 ZHU Shan-jun1 ZHU Zhi-m ing2 HU Hou-xiang2DING Gang 2
1.Department of Cardiology, Xinqiao Hospital, 2.Hypertension Center,Daping Hospital, Third Military Medical University, Chongqing 400037, China
关键词:
丝裂素活化蛋白激酶 心肌细胞 细胞肥大 钙激动剂
Keywords:
mitogen activated protein kinase cardiomyocytes cell hypertrophy calclum activato
分类号:
R329.28
DOI:
-
文献标识码:
A
摘要:
目的 探讨不同来源的细胞内钙( [Ca2+ ]i) 对心肌细胞丝裂素活化蛋白激酶(MA K) 介导的心肌细胞肥大反应的作用。方法 以培养的大鼠心肌细胞为模型, 用血管紧张素Ⅱ (AngⅡ ) 刺激心肌细胞外Ca2+ 跨膜内流、三磷酸肌醇( IP3) 刺激胞内Ca2+ 释放, C232P2ATP 掺入法和免疫印迹(westernblot) 测MA PK 活性及蛋白含量, 氚2亮氨酸(3H2Leu)、氚2胸腺嘧啶(3H2TdR) 掺入量作为心肌细胞肥大的指标。结果 AngⅡ , IP3 刺激15min 均能显著增加心肌细胞MAPK 活性及蛋白含量, 并提高3H2Leu, 3H2TdR 掺入量, 与对照组心肌细胞相比差异显著(P<0.01)。结论 钙激动剂诱导的MAPK 活性及含量的增加参与了心肌细胞肥大, 心肌细胞的肥大与[Ca2+ ]i 的来源无关。
Abstract:
AIM To investigate the effect of intracellular free calcium ([Ca2+]i) from different sources on the hypertrophy of cardiomyocytes mediated by mitogen activated protein kinase (MAPK).METHDOS Calcium influx was stimulated with angiotensionⅡ(AngⅡ),calcium was released with inositol-(1, 4, 5)-trisphosphate (IP3) in cultured rat ardiomyocytes, MAPK activity and MAPK protein expression were measured byγ-32P-ATP incorporation and by western blot respectively; cardiomyocytes hypertrophy was marked by3H-Leucine (3H-Leu) and3H-Thymidine(3H-TdR) incorporations.RESULTS AngⅡand IP3could increase MAPK activity and MAPK protein content,and promote3H-Leu and3H-TdR incorporations in cardiomyocytes,which were significantly different from those of the controlled cardiomyocytes (P< 0. 01 ).CONCLUSION cardiomyocyte proliferation closely related with the [Ca2+]iconcentration.

参考文献/References

[1] Dolmetsch RE, Lewis RS, Goodnow CC,et al. Differential activation of transcription factors induced by Ca2+response amplitude and duration[J].Nature,1997,386(6627):855.

[2] Bers DM,Perez-Reyes E. Ca2+channels in cardiac myocytes:structure and function in Ca2+influx and intracellular Ca2+ release[J].Cardiovasc Res, 1999, 42(2):339.

[3] Anger M,Lompre AM,Vallot O,et al. Cellular distribution of Ca2+release in channels in rat cardiac hypertrophy induced by aortic stenosis[J].Circulation,1998,98(22):2477.

[4] Lee HW, Eghbali-Webb M. Estrogen enhances proliferative capacity of cardiac fibroblasts by estrog receptor-and mitogen-activated protein kinase-dependent pathways[J].J Mol Cell Cardiol,1998.30(7):1359.

[5] Li TC, Pang YZ, Tang CS. Determination for activity of mitogen-activated protein kinase[J].Bas Med Sci Clin,1996, 16(3):155-158.

[6] Rabikin SW, Sunga PS, Sanghera JS,et al. Reduction of angiotensinⅡ-induced activation of mitogen-activated protein kinase in cardiac hypertrophy[J].Cell Mol Life Sci,1997,53(11):955.

[7] Meghji P,Nazir SA,Dick DJ,et al. Regional workload induced changes in electrophysiology and immediate early gene expression in intact in situ porcine heart [J].J Mol Cell Cardiol,1997,29(11):3147.

[8] Lijnen P,Petrov V. Renin-angiotensin system, hypertrophy and gene expression in cardiac myocytes[J].J Mol Cell cardiol, 1999,31(5):949.

备注/Memo

备注/Memo:
收稿日期:2000-07-10.基金项目: 国家自然科学基金资助项目(No. 39970304) ; 重庆市科委资助项目
更新日期/Last Update: 2002-07-01