| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
B improves cardiac function and survival after myocardial infarction
1 Kyushu University Graduate School of Medical Sciences, Department of Cardiovascular Medicine, Fukuoka, Japan
2 Hokkaido University Graduate School of Medicine, Department of Cardiovascular Medicine, Sapporo, Japan
* To whom correspondence should be addressed. E-mail: kubotat{at}cardiol.med.kyushu-u.ac.jp.
NF-
B is a key transcription factor that regulates inflammatory processes. In the present study, we tested the hypothesis that blockade of NF-B ameliorate cardiac remodeling and failure after myocardial infarction (MI). Knock-out mice with targeted disruption of the p50 subunit of NF-B (KO) were used to block the activation of NF-B. MI was induced by ligation of the left coronary artery in male KO and age-matched wild-type (WT) mice. NF-B was activated in non-infarct as well as infarct myocardium in WT+MI mice, while the activity was completely abolished in KO mice. Blockade of NF-B significantly reduced early ventricular rupture after MI and improved the survival by ameliorating congestive heart failure. Echocardiographic and pressure measurement revealed that left ventricular fractional shortening and + dP/dtmax were significantly increased and end-diastolic pressure was significantly decreased in KO+MI mice compared to WT+MI mice. Histological analysis demonstrated significant suppression of myocyte hypertrophy as well as interstitial fibrosis in non-infarct myocardium in KO+MI mice. Blockade of NF-B did not ameliorate expression of proinflammatory cytokines in infarct or non-infarct myocardium. In contrast, phosphorylation of c-Jun N-terminal kinase was almost completely abolished in KO+MI mice. The present study demonstrates that targeted disruption of the p50 subunit of NF-B reduces ventricular rupture as well as improves cardiac function and survival after MI. Blockade of NF-B might be a new therapeutic strategy to attenuate cardiac remodeling and failure after MI.
This article has been cited by other articles:
|
|
 |
|
  S. Mahmoodzadeh, S. Fritschka, E. Dworatzek, T. H. Pham, E. Becher, A. Kuehne, M. M. Davidson, and V. Regitz-Zagrosek Nuclear Factor-{kappa}B Regulates Estrogen Receptor-{alpha} Transcription in the Human Heart J. Biol. Chem., September 11, 2009; 284(37): 24705 - 24714. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Pautz, P. Rauschkolb, N. Schmidt, J. Art, M. Oelze, P. Wenzel, U. Forstermann, A. Daiber, and H. Kleinert Effects of nitroglycerin or pentaerithrityl tetranitrate treatment on the gene expression in rat hearts: evidence for cardiotoxic and cardioprotective effects Physiol Genomics, July 9, 2009; 38(2): 176 - 185. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Hikoso, O. Yamaguchi, Y. Nakano, T. Takeda, S. Omiya, I. Mizote, M. Taneike, T. Oka, T. Tamai, J. Oyabu, et al. The I{kappa}B Kinase {beta}/Nuclear Factor {kappa}B Signaling Pathway Protects the Heart From Hemodynamic Stress Mediated by the Regulation of Manganese Superoxide Dismutase Expression Circ. Res., July 2, 2009; 105(1): 70 - 79. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. X. L. Liu, R. Tian, H. Baskind, W. Hsueh, and I. G. De Plaen Platelet-activating factor induces the processing of nuclear factor-{kappa}B p105 into p50, which mediates acute bowel injury in mice Am J Physiol Gastrointest Liver Physiol, July 1, 2009; 297(1): G76 - G81. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Frantz and J. Bauersachs Regarding the Article by Timmers et al Circ. Res., June 5, 2009; 104(11): e60 - e60. [Full Text] [PDF]
|
|
|
|
|
|
L. Timmers, J. K. van Keulen, I. E. Hoefer, M. F.L. Meijs, B. van Middelaar, K. den Ouden, C. J.A. van Echteld, G. Pasterkamp, and D. P.V. de Kleijn Targeted Deletion of Nuclear Factor {kappa}B p50 Enhances Cardiac Remodeling and Dysfunction Following Myocardial Infarction Circ. Res., March 13, 2009; 104(5): 699 - 706. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L Kao, W. Browder, and C. Li Cellular Cardiomyoplasty: What Have We Learned? Asian Cardiovasc Thorac Ann, January 1, 2009; 17(1): 89 - 101. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-L. Li, M.-L. Zhuo, D. Wang, A.-B. Wang, H. Cai, L.-H. Sun, Q. Yang, Y. Huang, Y.-S. Wei, P. P. Liu, et al. Targeted Cardiac Overexpression of A20 Improves Left Ventricular Performance and Reduces Compensatory Hypertrophy After Myocardial Infarction Circulation, April 10, 2007; 115(14): 1885 - 1894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Onai, J.-i. Suzuki, Y. Maejima, G. Haraguchi, S. Muto, A. Itai, and M. Isobe Inhibition of NF-{kappa}B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H530 - H538. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
