Regulating the regulator:: NF-κB signaling in heart

被引:164
作者
Hall, Gentzon
Hasday, Jeffery D.
Rogers, Terry B.
机构
[1] Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Dept Med, Div Pulm & Crit Care Med, Baltimore, MD 21201 USA
[3] Univ Maryland, Mucosal Biol Res Ctr, Baltimore, MD 21201 USA
[4] Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Inst Mol Cardiol, Baltimore, MD 21201 USA
关键词
nuclear factor-kappa B; cardiomyocyte; post-translational modification; heart disease; inflammation;
D O I
10.1016/j.yjmcc.2006.07.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The Nuclear Factor-kappa B (NF-kappa B) signaling pathway has been linked to several pathologic processes in the myocardium including cardiomyocyte proinflammatory cytokine release, ischemia/reperfusion injury, hypertrophy and apoptosis. However, very little is known about the intracellular mechanisms that govern NF-kappa B activity in the myocardial cells. Recent advances in our understanding of the regulation of NF-kappa B signaling in non-myocyte systems suggest that the activity of the NF-kappa B pathway is tightly regulated by a diversity of stress-activated signaling intermediates through direct post-translational modification of various components of the NF-kappa B pathway. In this review, we will focus on these recent revelations and their implications not only in cardiac pathologies, but in the development of new therapeutic strategies to manage heart disease. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:580 / 591
页数:12
相关论文
共 179 条
[11]   Activation of nuclear factor κB and bcl-x survival gene expression by nerve growth factor requires tyrosine phosphorylation of IκBα [J].
Bui, NT ;
Livolsi, A ;
Peyron, JF ;
Prehn, JHM .
JOURNAL OF CELL BIOLOGY, 2001, 152 (04) :753-763
[12]   Diverse effects of BCL3 phosphorylation on its modulation of NF-κB p52 homodimer binding to DNA [J].
Bundy, DL ;
McKeithan, TW .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (52) :33132-33139
[13]   Phosphorylation of serine 468 by GSK-3β negatively regulates basal p65 NF-κB activity [J].
Buss, H ;
Dörrie, A ;
Schmitz, ML ;
Frank, R ;
Livingstone, M ;
Resch, K ;
Kracht, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (48) :49571-49574
[14]   Casein kinase II-mediated phosphorylation of NF-κB p65 subunit enhances inducible nitric-oxide synthase gene transcription in vivo [J].
Chantôme, A ;
Pance, A ;
Gauthier, N ;
Vandroux, D ;
Chenu, J ;
Solary, E ;
Jeannin, JF ;
Reveneau, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (23) :23953-23960
[15]   Acetylation of ReIA at discrete sites regulates distinct nuclear functions of NF-κB [J].
Chen, LF ;
Mu, YJ ;
Greene, WC .
EMBO JOURNAL, 2002, 21 (23) :6539-6548
[16]   Regulation of distinct biological activities of the NF-κB transcription factor complex by acetylation [J].
Chen, LF ;
Greene, WC .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2003, 81 (09) :549-557
[17]   Nitric oxide:: An inhibitor of NF-κB/Rel system in glial cells [J].
Colasanti, M ;
Persichini, T .
BRAIN RESEARCH BULLETIN, 2000, 52 (03) :155-161
[18]   The cytoprotective effects of the glycoprotein 130 receptor-coupled cytokine, cardiotrophin-1, require activation of NF-κB [J].
Craig, R ;
Wagner, M ;
McCardle, T ;
Craig, AG ;
Glembotski, CC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (40) :37621-37629
[19]   Cardiac-specific abrogation of NF-κB activation in mice by transdominant expression of a mutant IκBα [J].
Dawn, B ;
Xuan, YT ;
Marian, M ;
Flaherty, MP ;
Murphree, SS ;
Smith, TL ;
Bolli, R ;
Jones, WK .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2001, 33 (01) :161-173
[20]   NITRIC-OXIDE DECREASES CYTOKINE-INDUCED ENDOTHELIAL ACTIVATION - NITRIC-OXIDE SELECTIVELY REDUCES ENDOTHELIAL EXPRESSION OF ADHESION MOLECULES AND PROINFLAMMATORY CYTOKINES [J].
DECATERINA, R ;
LIBBY, P ;
PENG, HB ;
THANNICKAL, VJ ;
RAJAVASHISTH, TB ;
GIMBRONE, MA ;
SHIN, WS ;
LIAO, JK .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (01) :60-68