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|本期目录/Table of Contents|

细胞外信号调节激酶的变化在心力衰竭患者心肌重构中的意义(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第1期
页码:
62-64
栏目:
临床研究
出版日期:
2006-01-01

文章信息/Info

Title:
Activation of extracellular signal regulated kinase in myocardial remodeling in patients with congestive heart failure
作者:
杨丽霞; 王先梅;  石燕昆; 郭传明;  齐峰;  任丽
成都军区昆明总医院心血管内科，云南 昆明 650032
Author(s):
YANG Li-xia;  WANG Xian-mei;  SHI Yan-kun; GUO Chuan-ming;  QI Feng;  REN Li
Department of Cardiology of Kunming General Hospital ,Chengdu Military Area, Kunming, Yunnan 650032, China
关键词:
心力衰竭; 充血性;  心肌重构 ; 细胞外信号调节激酶
Keywords:
heart failure;  congestive;  myocardial remodeling;  extracellular signal regulated kinase
分类号:
R541.6
DOI:
-
文献标识码:
A
摘要:
目的 了解慢性心力衰竭(CHF)患者心肌组织细胞外信号调节激酶（ERK）的变化与心肌重构和心功能的关系。方法 采用Western blot技术测定31例瓣膜病所致CHF患者不同心功能组心肌细胞ERK蛋白基础表达和激活情况。结果 瓣膜病所致CHF患者心肌组织呈心肌重构的病理改变，轻度CHF患者ERK基础表达受抑，激活的磷酸化ERK显著增高。重度CHF患者ERK蛋白大多以无活性的形式存在，激活降低。结论 ERK表达与CHF患者心肌重构和心功能关联密切，重度CHF患者较轻度患者心肌组织的磷酸化ERK活性显著降低。
Abstract:
AIM To explore the roles of myocardial cellular signaling transduction pathways via activations extracellular signal regulated kinase (ERK) in the failing heart，myocardial remodeling and cardiac function in patients with congestive heart failure (CHF). METHODS Pathologic and morphologic changes of myocardial tissue in 31patients with CHF caused by valvular heart disease and 5 normal subjects were observed under optical and electronic microscope. Expression of ERK and phospholatedERK in myocardial tissue were examined using western blot assay. RESULTSPathological studies showed typical myocardial remodeling in CHF patients with valvular heart disease. Alterations in MAPKs signaling pathway in myocardium of CHF were observed. Activation of ERK was obvious in mild CHF. CONCLUSION The expression of phospholatedERK protein is markedly increased in mild CHF patients than in severe CHF, indicating that there is a close relationship between expression of ERK protein and cardiac remodeling and cardiac function.

参考文献/References

［1］ Hunter JJ, Chien KR. Signal pathways for cardiac hypertrophy and failure［J］. New Engl J Med, 1999, 341: 1276-1283.

［2］ Ruwhof C, van der Laarse A. Mechanical stressinduced cardiac hypertrophy: mechanisms and signal transduction pathways［J］. Cardiocvasc Res,2000, 47: 23-37.

［3］ Sambrook J, Fritsch EF, Maniatis T.分子克隆实验指南［M］. 第2版. 北京：科学出版社，1996.

［4］ 沈文锦.慢性心力衰竭治疗研究的新目标［J］.心脏杂志，2003，15（5）：464-466.

［5］ Colucci WS. Molecular and cellular mechanisms of myocardial failure［J］. Am J Cardiol,1997, 80: L15-L25.

［6］ Adams JW, Sokata Y, Davis MG， et al. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apopotic heart failure［J］. Proc Natl Acad Sci USA, 1998, 95: 10140-10145.

［7］ Bogoyevitch MA, Ketterman AJ, Sugden PH. Cellular stresses differentially active cJun Nterminal protein kinases and extracellular signalregulated protein kinases in cultured ventricular myocytes［J］. J Biol Chem,1995, 270: 29710-29717.

［8］ Hill CS, Treisman R. Transcriptional regulation by extracellular signals: mechanisms and specificity［J］. Cell,1995, 270: 389-393.

［9］ Liang FQ, Lu S, Gardner DG. Endothelindependent andindependent compinents of strainactivated brain natriuretic peptide gene transcription require extracellular signal regulated kinase and p38 mitogenactivated protein kinase［J］. Hypertension,2000, 35: 188-192.

备注/Memo

备注/Memo:
收稿日期：2004-08-09.作者简介：杨丽霞，主任医师，博士 Tel：（0871）4074573 Email：dylixia＠126.com
更新日期/Last Update: