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牵张激活通道对膨胀心室大鼠原癌基因cfos表达的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第5期
页码:
428-430
栏目:
基础研究
出版日期:
2005-10-05

文章信息/Info

Title:
Effect of stretchactivated channels on ventricular dilationinduced cfos expression in rats
作者:
李莉1; 2;  程龙献1;  廖玉华1
1.华中科技大学同济医学院附属协和医院心内科，湖北 武汉，430022; 2.武汉大学人民医院心内科，湖北 武汉 430060
Author(s):
LI Li ; CHENG Longxian ; LIAO Yuhua
Department of Cardiology , Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430022
关键词:
牵张激活通道; cfos; 牵张
Keywords:
stretchactivated channels ;  cfos ;  stretch
分类号:
R331.31
DOI:
-
文献标识码:
A
摘要:
目的 研究牵张心室时牵张激活通道（SACs）对心肌细胞表达原癌基因cfos的影响。方法 离体灌流大鼠心脏并膨胀左心室30 min，停止灌流剪下左心室，抽提组织总RNA行半定量RTPCR，探讨牵张左室对心室细胞表达cfos的影响及SACs在其中的可能作用。结果 RTPCR结果示，在同样牵张力度及持续时间膨胀心室的条件下，牵张加链霉素组cfos表达水平明显低于无链霉素组。结论 SACs通道阻断剂－链霉素对膨胀左室致cfos表达有明显抑制作用，间接说明心室膨胀经SACs激活胞内信号诱导cfos表达；同时链霉素并不能完全抑制cfos表达，提示膨胀心室致cfos表达进而引起心室肥厚尚有其他传导途径，仍需进一步研究。
Abstract:
AIM To investigate the effects of stretchactivated channels (SACs) on ventricular cfos expression. METHODS Isolated normal adult rat hearts were perfused and streched by Langendorff method. The left ventricles were cut off after 30 min reperfusion. The total RNA was extracted for RTPCR to determine cfos expression. RESULTS The level of cfos expression in streptomycin group was significantly lower than that of the group without streptomycin. CONCLUSION Streptomycin, a blocker of SACs, can partially inhibit left ventricular dilationinduced cfos expression, impling that SACs may be one of the pathways to induce cfos expression and ventricular hypertrophy.

参考文献/References

［1］ Christiane D, Thienelt BS, Ellen O, et al. Loadinduced growth responses in isolated adult rat hearts［J］. Circulation, 1997,95:2677-2683.

［2］ Christina M, William M. Mechanotransduction via the elastinlaminin receptor in resistance arteries［J］. J Biomechanics, 2003,36:645-652.

［3］ McBride TA. Stretchactivated ion channels and cfos expression remain active after repeated eccentric bouts［J］. J Appl Physiol, 2003,94(6):2296-2302.

［4］ Reiter MJ, Synhorst DP, Mann DE. Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart［J］. Circ Res, 1998,62:554-562.

［5］ Van Wamel AJ, Ruwhof C, Van der ValkKokshoorn LE. Rapid gene transcription induced by stretch in cardiac myocytes and fibroblasts and their paracrine influence［J］. Eur J Physiol, 2000,439:781-788.

［6］ 冯瑗, 叶本兰. 机械敏感性钾通道及其在心肌肥大中的信号转导机制［J］. 心脏杂志, 2004, 16(1):73-75.

［7］ Andrew HJ, Joseph L, Geoff R, et al. Effect of streptomycin on wallstressinduced arrhythmias in the working rat heart［J］. Cardiovasc Res, 1997,34:493-503.

［8］ Hautala N, Tenhunen O, Szokodi I. Direct left ventricular wall stretch activates GATA4 binding in perfused rat heart: involvement of autocrine/paracrine pathways［J］. Pflügers Arch, 2002,443(3):362369.

［9］ Van Wamel AJ, Ruwhof C, Van Der ValkKokshoom LE, et al. The role of angiotensin II, endothelin1 and transforming growth factorbeta as autocrine/paracrine mediators of stretchinduced cardiomyocyte hypertrophy［J］. Mol Cell Biochem， 2001，218(12):113-124.

备注/Memo

备注/Memo:
收稿日期：2004-02-23.基金项目：国家自然科学基金资助（No.30270559）
更新日期/Last Update: 2010-01-05