Changes in gene expression induced by H2O2 in cardiac myocytes

被引:62
作者
Kemp, TJ
Causton, HC
Clerk, A [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, NHLI Div Cardiac Med, Fac Med, London, England
[2] Univ London Imperial Coll Sci Technol & Med, CSC IC Microarray Ctr, Fac Med, London, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
oxidative stress; cardiac myocytes; microarrays; gene expression; p21(Cip1/Waf1); heat shock protein; heme oxygenase; syndecan;
D O I
10.1016/S0006-291X(03)01215-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress induces cardiac myocyte apoptosis. At least some effects are probably mediated through changes in gene expression. Using Affymetrix arrays, we examined the changes in gene expression induced by H2O2 (0.04, 0.1, and 0.2 mM; 2 and 4h) in rat neonatal ventricular myocytes. Changes in selected upregulated genes were confirmed by ratiometric RT-PCR. p21(Cipl/Wafl) was one of the only two genes upregulated in all conditions studied. Of the heat shock proteins, only Hsp70/70.1 was induced by H2O2 with no change in the expression of Hsp25, Hsp60 or Hsp90. Heme oxygenase 1 was also potently upregulated, but not heme oxygenases 2 or 3. Of the intercellular adhesion proteins, syndecan-1 was significantly upregulated in response to H2O2, with little change in the expression of other syndecans and no change in expression of any of the integrins studied. Thus, oxidative stress, exemplified by H2O2, selectively promotes the expression of specific gene family members. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:416 / 421
页数:6
相关论文
共 23 条
[1]   H2O2 induces a transient multi-phase cell cycle arrest in mouse fibroblasts through modulating cyclin D and p21Cip1 expression [J].
Barnouin, K ;
Dubuisson, ML ;
Child, ES ;
de Mattos, SF ;
Glassford, J ;
Medema, RH ;
Mann, DJ ;
Lam, EWF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (16) :13761-13770
[2]   Stress (heat shock) proteins - Molecular chaperones in cardiovascular biology and disease [J].
Benjamin, IJ ;
McMillan, DR .
CIRCULATION RESEARCH, 1998, 83 (02) :117-132
[3]   ACTIVATION OF THE MITOGEN-ACTIVATED PROTEIN-KINASE CASCADE BY PERTUSSIS-TOXIN-SENSITIVE AND PERTUSSIS-TOXIN-INSENSITIVE PATHWAYS IN CULTURED VENTRICULAR CARDIOMYOCYTES [J].
BOGOYEVITCH, MA ;
CLERK, A ;
SUGDEN, PH .
BIOCHEMICAL JOURNAL, 1995, 309 :437-443
[4]   CELLULAR PRODUCTION OF HYDROGEN-PEROXIDE [J].
BOVERIS, A ;
CHANCE, B ;
OSHINO, N .
BIOCHEMICAL JOURNAL, 1972, 128 (03) :617-&
[5]   Regulation of cardiac myocyte cell death [J].
Clerk, A ;
Cole, SM ;
Cullingford, TE ;
Harrison, JG ;
Jormakka, M ;
Valks, DM .
PHARMACOLOGY & THERAPEUTICS, 2003, 97 (03) :223-261
[6]   Up-regulation of c-jun mRNA in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-Jun N-terminal kinases are required for efficient up-regulation of c-Jun protein [J].
Clerk, A ;
Kemp, TJ ;
Harrison, JG ;
Mullen, AJ ;
Barton, PJR ;
Sugden, PH .
BIOCHEMICAL JOURNAL, 2002, 368 (01) :101-110
[7]  
Cook SA, 1999, CIRC RES, V85, P940
[8]   New roles for p21 and p27 cell-cycle inhibitors: a function for each cell compartment? [J].
Coqueret, O .
TRENDS IN CELL BIOLOGY, 2003, 13 (02) :65-70
[9]  
FERRARI R, 1998, EUR HEART J, V19, P2
[10]   Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium [J].
Ide, T ;
Tsutsui, H ;
Kinugawa, S ;
Suematsu, N ;
Hayashidani, S ;
Ichikawa, K ;
Utsumi, H ;
Machida, Y ;
Egashira, K ;
Takeshita, A .
CIRCULATION RESEARCH, 2000, 86 (02) :152-157