Expression of p22-phox and gp91-phox, essential components of NADPH oxidase, increases after myocardial infarction

被引:97
作者
Fukui, T
Yoshiyama, M
Hanatani, A
Omura, T
Yoshikawa, J
Abe, Y
机构
[1] Kagawa Med Univ, Dept Pharmacol, Kagawa 7610793, Japan
[2] Osaka City Univ, Dept Med, Div Cardiol, Osaka 558, Japan
关键词
NADPH oxidase; superoxide anion; ventricular remodeling; lipid peroxidation; NF-kappa B; oxidative stress;
D O I
10.1006/bbrc.2001.4493
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
Recent studies have shown that oxidative stress plays an important role in cardiovascular diseases. NADPH oxidase is one of the major sources of superoxide anions and a candidate for the initiation and development of atherosclerosis, which involves the remodeling of vasculature. However, the relevance of NADPH oxidase in ventricular remodeling has not been well-characterized. This is the first report showing that the expression of p22-phox and gp91-phox, essential components of NADPH oxidase, are increased in the infarcted sites after myocardial infarction. The levels of thiobarbituric acid reactive substance, which indicates the lipid peroxidation level, and nuclear factor-kappaB (NF-kappaB) DNA binding activity are also increased in infarcted sites. Our results suggest that the increased expression of NADPH oxidase may have an effect on left ventricular remodeling by increasing the redox-sensitive NF-kappaB DNA binding activity as well as the lipid peroxidation level. (C) 2001 Academic Press.
引用
收藏
页码:1200 / 1206
页数:7
相关论文
共 32 条
[11]  
Griendling KK, 1997, CIRCULATION, V96, P3264
[12]   INHIBITION BY ANGIOTENSIN-II TYPE-1 RECEPTOR ANTAGONIST OF CARDIAC PHENOTYPIC MODULATION AFTER MYOCARDIAL-INFARCTION [J].
HANATANI, A ;
YOSHIYAMA, M ;
KIM, SK ;
OMURA, T ;
TODA, I ;
AKIOKA, K ;
TERAGAKI, M ;
TAKEUCHI, K ;
IWAO, H ;
TAKEDA, T .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (09) :1905-1914
[13]   Cellular and molecular mechanisms of endothelial cell dysfunction [J].
Harrison, DG .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (09) :2153-2157
[14]  
Hill MF, 1996, AM J PATHOL, V148, P291
[15]   Polymorphism of the NADH/NADPH oxidase p22 phox gene in patients with coronary artery disease [J].
Inoue, N ;
Kawashima, S ;
Kanazawa, K ;
Yamada, S ;
Akita, H ;
Yokoyama, M .
CIRCULATION, 1998, 97 (02) :135-137
[16]   INTERPRETATION OF THE THIOBARBITURIC ACID REACTIVITY OF RAT-LIVER AND BRAIN HOMOGENATES IN THE PRESENCE OF FERRIC ION AND ETHYLENEDIAMINETETRAACETIC ACID [J].
KIKUGAWA, K ;
KOJIMA, T ;
YAMAKI, S ;
KOSUGI, H .
ANALYTICAL BIOCHEMISTRY, 1992, 202 (02) :249-255
[17]  
Kinugawa S, 2000, CIRC RES, V87, P392
[18]   Increased activity of nuclear factor-κB participates in cardiovascular remodeling induced by chronic inhibition of nitric oxide synthesis in rats [J].
Kitamoto, S ;
Egashira, K ;
Kataoka, C ;
Koyanagi, M ;
Katoh, M ;
Shimokawa, H ;
Morishita, R ;
Kaneda, Y ;
Sueishi, K ;
Takeshita, A .
CIRCULATION, 2000, 102 (07) :806-812
[19]   Interactions between the components of the human NADPH oxidase: Intrigues in the phox family [J].
Leusen, JHW ;
Verhoeven, AJ ;
Roos, D .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1996, 128 (05) :461-476
[20]   In vivo transfection of cis element ''decoy'' against nuclear factor-kappa B binding site prevents myocardial infarction [J].
Morishita, R ;
Sugimoto, T ;
Aoki, M ;
Kida, I ;
Tomita, N ;
Moriguchi, A ;
Maeda, K ;
Sawa, Y ;
Kaneda, Y ;
Higaki, J ;
Ogihara, T .
NATURE MEDICINE, 1997, 3 (08) :894-899